Path_ggf_6d - School of Life Sciences

Prothrombin Time Blood Test-PT
This test is done to evaluate the blood for its
ability to clot. It is often done before surgery
to evaluate how likely the patient is to have
a bleeding or clotting problem during or
after surgery.
Normal PT Values: 10-12 seconds (this can
vary slightly from lab to lab)
Common causes of a prolonged PT include
vitamin K deficiency, hormones drugs including
hormone replacements and oral contraceptives,
disseminated intravascular coagulation (a
serious clotting problem that requires immediate
intervention), liver disease, and the use of the
anti-coagulant drug warfarin. Additionally, the
PT result can be altered by a diet high in vitamin
K, liver, green tea, dark green vegetables and
Partial Thromboplastin Time Blood Test-PTT
This test is performed primarily to determine if
heparin (blood thinning) therapy is effective. It
can also be used to detect the presence of a
clotting disorder. It does not show the effects of
drugs called “low molecular weight heparin” or
most commonly by the brand name Lovenox.
Normal PTT Values: 30 to 45 seconds (this
can value slightly from lab to lab)
Extended PTT times can be a result of
anticoagulation therapy, liver problems, lupus
and other diseases that result in poor clotting.
INR=(PT patient/PT normal)ISI
PT patient = patient's measure PT
PT normal = laboratory's
geometric mean value for normal
patients (seconds)
ISI = International Sensitivity Index
International Normalized Ratio Blood
Normal INR Values: 1 to 2
The INR is used to make sure the results
from a PT test is the same at one lab as it
is at another lab. In the 1980’s the World
Health Organization determined that
patients may be at risk because the results
of a PT test would vary from one lab to
another, based upon the way the test was
done. The “normal” range for one lab
would be different than a “normal” value
from another lab, creating problems for
patients who were being treated in several
locations. In order to standardize the
results between labs, the INR was created.
The INR result should be the same,
regardless of the location where the tests
are performed.
Figure 3 Action of LMWHs on the traditional coagulation cascades, showing
coagulation factors PKK and HMWK
Davenport, A. (2011) What are the anticoagulation options for intermittent hemodialysis?
Nat. Rev. Nephrol. doi:10.1038/nrneph.2011.88
D-dimer is the degradation product of
crosslinked (by factor XIII) fibrin.
It reflects ongoing activation of the hemostatic
Extravasation of blood into the extravascular
Capillary bleeding can occur under
conditions of chronic congestion.
Rupture of a large artery or vein results in
severe hemorrhage and is almost always
due to vascular injury, including trauma,
atherosclerosis, or inflammatory or
neoplastic erosion of the vessel wall.
Capillary Bleeding
• Extravasation of blood due to ruptured
 From hemo = blood, rrhagia = to burst forth
• Hemorrhage may be external or internal
• Hemorrhage may be obvious (gross) or
hidden (occult)
• This is whole blood with RBCs, not just
edemic transudates or exudates
Hemorrhage may be external or contained within a tissue.
Any accumulation is called a hematoma.
Hematomas may be relatively insignificant or so massive that death ensues.
The Ocular Pathology of Terson's Syndrome
Subcapsular Hematoma
Minute 1- to 2-mm hemorrhages
into skin, mucous membranes,
or serosal surfaces are called
These are most commonly
associated with locally
increased intravascular
pressure, low platelet counts
(thrombocytopenia), or defective
platelet function (as in uremia).
Petechiae from Strangulation
Figure 3Kinetics of inflammatory
bleeding in thrombocytopenic mice
during reverse passive Arthus reaction.
(A) Photographs of progressing rpA in the
dorsal skinfold chamber. In the absence of
platelets, petechial bleeding was clearly
visible after 2 hours and increased with
time. In nondepleted animals there were
virtually no petechial spots. Window
diameter was 12 mm. (B) Microscopic view
of the progressing rpA in a
thrombocytopenic mouse. Petechial
bleeding was detected at 20 minutes, with
further growth of the spot at 40 minutes.
Bar = 200 μm. (C) Petechial spots visible
to the eye (∼ 100 μm) were counted during
rpA in thrombocytopenic and control
animals. The difference in incidence of
petechiae became statistically significant
within 1 hour (P < .01; n = 4). At t = 4
hours, the petechiae became confluent,
impairing quantification. Error bars
represent SEM.
Slightly larger (≥3 mm) hemorrhages
are called purpura.
Figure 2: Microscopic examination of palpable purpura. Severe pandermal
leucocytoclastic vasculitis without granulation (HE, original magnification ×40; inset:
These may be associated with many of
the same disorders that cause
petechiae or can be secondary to
trauma, vascular inflammation
(vasculitis), or increased vascular
fragility (e.g., in amyloidosis).
The below is still in draft form
Larger (>1 to 2 cm) subcutaneous hematomas
(i.e., bruises) are called ecchymoses.
The red cells in these lesions are degraded and
phagocytized by macrophages; the hemoglobin
(red-blue color) is then enzymatically converted
into bilirubin (blue-green color) and eventually into
hemosiderin (gold-brown color), accounting for the
characteristic color changes in a bruise.
Echymoses or contusions
Depending on the location, a large
accumulation of blood in a body cavity is
denoted as a hemothorax,
hemopericardium, hemoperitoneum, or
hemarthrosis (in joints).
Patients with extensive bleeding can
develop jaundice from the massive
breakdown of red cells and hemoglobin.
Indications of internal hemorrhage
• Deep
 Anemia—fewer circulating RBCs
 Increased indirect bilirubin (unconjugated,
• Surface
 Hemorrhage under the skin or mucous
membranes looks red (oxygenated Hb) or
purple (deoxygenated Hb)
Distribution of hemorrhage(s)
Multifocal indicates problem affecting vessels or platelets
 thrombocytopenia or thrombocytopathy
• reduced number or function of platelets preventing coagulation
 inherited coagulation defects—hemorrhagic diathesis
 anticoagulants inhibit production of vitamin K-dependent coagulation
 end stage hepatic disease.
• With approximately 80% loss of functional hepatic tissue, production of
coagulation factors can become inadequate.
 disseminated intravascular coagulation (DIC)
• coagulation out of control
 vasculitis
• immune mediated--precipitation of Ag-Ab complexes, which are chemotactic
for neutrophils, resulting in vascular damage
• infections of endothelium
Focal distribution
 single or a few focal hemorrhages are typical of trauma
 regional neoplasm, thrombosis, or microbial invasion
 problems with protein clotting factors
This is hemopericardium as demonstrated
by the dark blood in the pericardial sac
opened at autopsy. Penetrating trauma or
massive blunt force trauma to the chest
(often from the steering wheel) causes a
rupture of the myocardium and/or coronary
arteries with bleeding into the pericardial
cavity. The extensive collection of blood in
this closed space leads to cardiac
tamponade. A pericardiocentesis, with
needle inserted into the pericardial cavity,
can be a diagnostic procedure.
Gastrointestinal hemorrhage
• When rate is slow, blood is digested or lost
in feces
 In upper GI, blood turns black and tarry as it is
digested and is called melena
• Melena is symptomatic of peptic ulcers, ruptured
esophageal varices, cancers
 In lower GI, blood remains red and is excreted
with feces
• Fecal occult blood test; now fecal immunochemical
– FOBT used dye adsorbed on paper to detect Fenton
reaction catalyzed by heme iron
– FIT uses Ab against globin portion of hemoglobin
Hemorrhage into cavities
• Pleural hemorrhage—hemothorax
 Build-up of pressure prevents lung expansion
• Prevents gas exchange
• May lead to lung collapse
 Instigates coughing or hiccups, which exacerbates
• Pericardial hemorrhage—hemopericardium
 Build-up of external pressure inhibits filling
 Cardiac tamponade = compression
• Intracranial hemorrhage
 Always bad because of the rigid cranium
 CSF pressure increases rapidly if bleeding rate is
greater than rate of fluid resorption
• Maintenance of blood volume
• Maintenance of blood pressure
• Mainenance of clot-free flow
 plasmin
• Development of clot in response to
vascular damage—hemostasis
 thrombin-fibrin
Clotting v. thrombosis
• THROMBUS: Blood that has solidified
within the vascular lumens or cardiac
• CLOT: Blood that has solidified anywhere
thrombus that travels through the
vasculature to form a plug elsewhere
• EMBOLISM: vascular plug, not always
from a thrombus
Consequences of acute hemorrhage
• Loss of blood beyond a certain volume will cause
systemic hypotension
 rapid compensation by the baroreceptor response leads to
peripheral vasoconstriction
 fluids shift from the interstitial into the IV compartment
 slower response from the renin-angiotensin-aldosterone system
results in vasoconstriction and retention of sodium and water by
the kidney
 antidiuretic hormone (ADH) also kicks in, acts on nephron to
promote water resorption
• Loss of blood beyond the body's ability to compensate
will cause systemic hypotension, reduced cardiac filling,
reduced tissue perfusion, loss of erythrocytes and their
Hb, hypoxemia, and a further cascade of events called
Blood loss
• Class I: up to 15% of blood volume
 typically no change in vital signs
 routine blood donation amounts to ~10%
• Class I: 15-30% of total blood volume
 tachycardia (rapid heart beat) with a narrowing of the difference
between the systolic and diastolic blood pressures
 compensatory peripheral vasoconstriction; cool, pale skin;
altered mental status, dizzy or confused
 fluid resuscitation with saline or Lactated Ringer's solution
• Class III: 30-40% of circulating blood volume
 blood pressure drops, heart rate increases, peripheral perfusion
worsens, mental status worsens
 fluid resuscitation and/or blood transfusion
• Class IV: >40% of circulating blood volume
 hypovolemic shock--limit of the body's compensation is reached
 aggressive resuscitation is required to prevent death
Hypovolemic, cardiogenic shock
• Causes
Blood loss
Reduced cardiac output
Deranged peripheral vasomotor control
• Consequenses
 Inadequate perfusion
 Hypoxia, lactic acidosis
• Recovery dependent on duration and
Stages of Shock
• Early Stage
 Compensatory mechanisms maintain perfusion of
vital organs
 Include increased heart rate and increased peripheral
• Progressive Stage
 Compensatory systems no longer adequate with
tissue hypoperfusion
 Onset of circulatory and metabolic imbalance,
especially metabolic acidosis from lactic acidemia
• Irreversible Stage
 Organ damage and metabolic disturbances
 Survival not possible
Clinical consequences
Weak, rapid pulse (tachycardia)
Shallow rapid breathing (tachypnea)
Cool, damp, cyanotic skin
Tissue injuries are due to hypoxia

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