Disturbances in circulation pt2 Flashcards
Activation of the sympathetic nervous system produces (2) to redistribute blood to vital organs
- peripheral vasoconstriction
- tachycardia
Activation of the apneustic and pneumotaxic areas of the brain
Stimulation of the respiratory centers in the brain
Stimulation of adrenal gland releases these chemicals
- Adrenal medulla - catecholamines (epinephrine and norepinephrine)
- Adrenal cortex - glucocorticoids
result toconservation of sodium ions and water by increasing kidney tubular
reabsorption
Activation of the Renin-Angiotensin-Aldosterone Axis
Counter Regulatory Mechanisms operating at early stages of shock
- Activation of Sympathetic Nervous System
- Stimulation of the respiratory centers in the brain
- Stimulation of adrenal gland
- Activation of the Renin-Angiotensin-Aldosterone Axis
Hypovolemic Shock
includes hemorrhage and traumatic shock; inadequate blood or plasma volume
Cardiogenic Shock
shock resulting from myocardial infarction; failure of myocardial pump due to intrinsic myocardial damage
shock associated with toxemia and septicemia, including endotoxemia
septic or toxic shock
Neurogenic Shock
resulting from severe fright, pain and trauma without hemorrhage
as a result of massive degranulation of mast cells following antigen-antibody interaction
anaphylactic shock
Stages of shock
- Stage of ischemic hypoxia
- Stage of stagnant hypoxia
3.. Stage of irreversibility
(non-progressive phase) where there occurs reflex vasoconstriction in an attempt to maintain blood pressure and
cardiac output
stage of ischemic hypoxia
associated with gradual fading of pre-capillary vasoconstriction with pooling of blood in the capillary, a decline in venous return, and diminishing blood pressure
stagnant hypoxia
shift of fluid from the intravascular space to the extravascular space and microembolization of capillaries
stage of irreversibility
phase that the counter regulatory mechanisms are activated
stage of ischemic hypoxia
state of peripheral circulatory failure caused by sudden and severe injury
shock
shock is a syndrome of?
diminishing blood pressure in the capillary bed
anaerobic glycolysis results in accumulation of this acid which cause acidosis
Lactic acid/lactate
True or false.
Decrease in pH (as caused by accumulation of lactate) perpetuates the state of shock.
True. As pH decrease, ATP production decrease and extend state of shock.
DIC phase associated with subsequent formation of
thrombin
hypercoagulable phase
leads to platelet aggregation and fibrin formation resulting to microthrombosis of vascular capillaries, and infarction in many organs
hypercoagulable phase
Clotting factors depleted during hypocoagulable phase
- fibrinogen
- Factor VIII (anti-hemophilic factor)
- Factor V (proaccelerin)
associated with the activation of
the fibrinolytic system with consequent release of fibrin and fibrinogen
degradation products that suppresses fibrin polymerization
hypocoagulable phase
area of coagulative necrosis caused by ischemia and is due to obstruction of the blood supply following thrombosis or embolism
infarct
process of infarct called
infarction
cells and tissues most susceptible to infarction
▪ brain,
▪ renal tubular epithelia,
▪ heart muscles, and
▪ most parenchymal tissues
resistant to infarction such that the
stromal support of infracted tissues survives while the parenchyma succumb to
infarction
fibroblasts
artery ramifies into smaller branches as it ends
Functional End-Artery
Functional end artery organs where infarction are commonly seen
- kidneys
- heart muscles
- brain
- spleen
there are separate blood supply that often has several functional anastomotic channels
Parallel system
pulmonary and hepatic infarctions rarely occur but may happen if dual blood supply is compromised, such as in?
chronic passive venous congestion
organs that have two separate blood
supply originating from different points (dual blood supply)
- lungs (pulmonary artery and bronchial artery)
- liver (hepatic artery and portal vein)
thrombo-embolic colic in the horse is cause by ___ obstructing the
cranial mesenteric artery
Strongylus vulgaris
Thrombotic or embolic occlusion
rarely leads to infarction in organs with parallel system, but happens so when?
occlusion occurs at the root of the blood vessel
localized anemia
ischemia
ischemia results to infarction if it lodges in organs with so called
end arteries
if ischemia is partial or gradual it results to
atrophy
oxygenation of blood is normal, but the tissues cannot utilize oxygen due to damage to certain critical cellular respiratory processes such as that seen in cyanide poisoning
histotoxic anoxia
caused by low hemoglobin or reduced capacity of blood to carry oxygen as in carbon monoxide poisoning
anemic anoxia
result from insufficient oxygenation of blood as may occur in severe pneumonia
anoxic anoxia
ischemia due to reduced flow of oxygenated blood as in hypovolemic shock
stagnant anoxia
reduction of blood supplies maybe partial called
hypoxia
anoxia
complete reduction in the oxygen supplied to tissues
reduction in the flow of arterial blood to an organ or tissue result to
ischemia
end result of ischemia depend on
- organ involved
- degree of occlusion/anoxia
- presence of collateral circulation
- size of blood vessels
Causes of ischemia
- Compression of blood vessels
- Obstruction
- Functional lesion
stagnant anoxia example
hypovolemic shock
anoxic anoxia may occur in
severe pneumonia
Anemic Anoxia example
carbon monoxide poisoning
histotoxic anoxia example
cyanide poisoning
solid mass transported from one part of the body to another through the circulatory system
emboli
process of a solid mass being transported from one part of the body to another
through the circulatory system
embolism
embolus can be:
- fragments of thrombi
- fat cells
- tumor cells
- aggregates of bacteria and parasites
- bone marrow cells
- amniotic cells
- foreign bodies
produces emboli of pieces of skin or hair
venipuncture
One of the notorious “seeders” of emboli that causes multiple embolisms in the
kidneys
bacterial valvular endocarditis
Valvular thrombosis of the left chamber of the heart usually produces emboli in the
systemic circulation
valvular thrombosis in the left chamber of the heart cause emboli at the?
Systemic circulation
organs with end artery
brain, kidneys, spleen and myocardium
detachment of thrombi in the vessel wall can cause
emboli
thrombi become larger and larger eventually obstructing the lumen of the blood vessel where they are formed
propagation
portions of the thrombi break and
are carried into the circulation
fragmentation to form thrombo-emboli
lysis of the thrombi by plasma-derived
fibrinolytic system or through slow phagocytosis by phagocytic cells
dissolution by fibrinolysis
invasion and growth of fibrous tissue could happen, along with recanalization and restoration of blood flow
fibrous tissue organization
Once thrombi are formed, there are four possible outcomes
- Propagation
- Fragmentation to form thrombo-emboli
- Dissolution by fibrinolysis
- Fibrous tissue organization
Thrombi are clinically important for two reasons
a) they cause obstruction of blood vessels
b) they can be a source of emboli
in cat species, thrombosis at this site cause hind limb paralysis
distal aorta
in horse species, thrombosis at this site is usually caused by strongyle infection
cranial mesenteric arteries
trailing thrombi with one end attached and
the other freely moving
obturating thrombi
straddles the bifurcation of blood vessels
saddle thrombi
Canalized thrombi
allows partial flow of blood
Occluding thrombi
blocks the entire lumen of the blood vessel
Valvular thrombi
attached to the valves of the heart
Mural thrombi
attached to the endocardial wall of heart
Based on location of thrombi:
a. Cardiac thrombi
b. Arterial thrombi
c. Venous thrombi
d. Lymphatic thrombi
e. Capillary thrombi or hyaline thrombi
septic thrombi
contains bacteria
aseptic thrombi
no pathogenic agent present
parasitic thrombi
contains parasites such as filarial worms
red thrombi
composed of all blood cell components
pale or white thrombi
composed entirely of platelets
layered red and white thrombi
laminated or mixed thrombi
pale gray-tan mass consisting of bands of fibrin and platelets mixed with coagulated red blood cells
arterial thrombi
when arterial thrombi builds up, head and tail are in what colors?
Head - pale
Tail - darker red
During propagation concentric laminations are formed
lines of Zahn
they are dark red, moist or gelatinous and are easier to dislodge
venous thrombi
resemble intravascular clots of whole blood due to slow blood flow and as influenced by gravity
venous thrombi
It is the carbohydrate-rich cell coat present in endothelial lining cells which prevents circulating cells from adhering to the surface
glycocalyx
negatively-charged surface of
endothelial lining lead to a mutual electrostatic repulsion between two sets
of negatively charged cells
surface negativity theory
prostaglandin that prevent platelet
aggregation by converting platelet aggregation factors into unstable substances
Prostacyclin (PG12)
Theories on Non-thrombogenic Vascular Endothelia
- Glycocalyx theory
- Surface negative theory
- Surveillance system theory
prostacyclin convert these platelet aggregation factors to unstable forms
- endoperoxidase
- thromboxane A2
hemostasis steps
- vascular contraction
- stasis of blood
- endothelial adhesion
- blood coagulation
- platelet aggregation
formation of ante mortem clot within the blood vessels
thrombosis
2 mechanisms of blood coagulation
- intrinsic clotting mechanism
- extrinsic clotting mechanism
intrinsic clotting mechanism
involves the components normally present in the plasma
extrinsic clotting mechanism
involves tissue component in addition to the components from the blood