Friedenberg and Lab Basic Pathology Flashcards
Clinical diagnosis
from case history, clinical signs, and physical exam
etiology
cause of disease
can be intrinsic or extrinsic and be as specific as possible
differential diagnoses
lost of diagnoses that could account for the clinical signs or lesions
Components of morphological diagnosis
organ, process, process modifier, distribution, (duration, severity)
Most Likely diagnosis
greatest possibility based on the available evidence
description of pathological lesions
Visual, palpable, incision
Differentiation of tissue
lesion, postmortem artifact, variation of normal
focal
one location
multifocal
a few singular spots around
multifocal coalescing
spots around and some are close and forming together
widely disseminated
lots of spots all over the organ or tissue
locally extensive
clump of a lot in one area
diffuse
completely covered
segmental
large chunk one piece around cylinder
annular
small band around it cylinder
transmural
different lesions different ways when tube is cut
-itis
inflammation
4 major processes
degenerative/necrosis, inflammation/repair, circulatory disturbances, growth disturbances
sarcoma
malignant tumor of mesenchymal cell organs (muscle, bones, vascular)
Carcinoma
epithelial cells of the organs
fibroma
benign tumor of fibroblast
osteosarcoma
malignant tumor of osteoblasts
hepatocellular carcinoma
malignant tumor of hepatocytes
thrombosis
excessive coagulation (clotting) in blood
hemorrhage
deficient coagulation (clotting) in the blood
hemostasis 3
blood vessel wall, platelets, coagulation factors
Normal homeostasis
endothelium of vessels antagonize clot formation through:
vasodilation, inhibit platelet adhesion, aggregation, inhibit coagulation
Vascular injury 5 steps
1) vasoconstriction (decrease blood flow) with endothelin
2) primary hemostatic plug formation of platelets and subendothelial ECM
3) Tissue factor III triggers the coagulation cascade to make thrombin. This makes fibrinogen to fibrin forming over top as the SECONDARY HEMOSTATIC PLUG
4) anticoagulants released to protect from other coagulation in the body (fibrolysis).
5) clots eventually dissolve and are also very regulated
endothelium
antagonize or stimulate coagulation (the balance of this determines the physiological outcome)
either anticoagulant or procoagulant
Nitric oxide and prostacyclin PGI2
maintain vascular relaxation and inhibit adnesion and aggregation of platelets
adenosine-diphosphatase
an enzyme that degrades ADP (a stimulation of platelet aggregation)
Membrane associated heparin-like anticoagulants
potentiates the activity of antithrombin
antithrombin
potent anticoagulant
thrombomodulin
bonds to thrombin and converts it from a procoagulant to anticoagulant that activates protein C
protein C and S
vitamin K dependent factors that degrade coagulation factors
tissue plasminogen activator (t-PA)
promotes fibrinolysis
tissue factor pathway inhibitor (TFPI)
inactivates tissue factor VIIa complexes
von willibrand factor (vWF)
mediates platelet binding to subendothelial collagen and other surfaces
Tissue factor (Factor III)
initiates the coagulation cascade
Plasminogen activator inhibitors (PAIs)
inhibit fibrinolysis
Platelets forming primary hemostatic plug 4
adhesion, secretion, activation, aggregation
adhesion
platelets interact with vWF and creates a bridge between subendothelial ECM and platelet surface receptors
secretion
secrete alpha granules and dense bodies (release Ca that starts coag. cascade) and ADP to mediate Aggregation
activaton
expression of phospholipid complex on surface of platelets for Ca and coag. factor binding
aggregation
ADP and Thromboxane A2 (vasoconstrictors) cycle of platelets to make primary plug. (reversible until the coag. cascade and formation of thrombin have happened).
thrombin formation - makes platelet contraction and the secondary hemostatic plug as well as converts Fibrinogen to fibrin (cementing the platelets)
fibrinogen
links activated platelets to form large platelet aggregates with a receptor. the receptor is necessary or they could develop a bleeding disorder
platelet functions
wound healing, angiogenesis, metastasis of neoplasia
coagulation cascade
intrinsic and extrinsic pathways that converge to the common pathway
Initiation of coagulation
primarily through tissue factor activation of the extrinsic pathway
end result of coagulation cascade
thrombin and fibrinogen to fibrin (cross linked) forming a plug
Cell-based model
not what we use but is the more accurate coagulation cascade
extrinsic pathway
tissue factor (III) - Tissue factor VIIa - common pathway
Tissue factor initiates
VII produced in liver and Vit. K dependent (rodenticide toxicity this is the first to go)
intrinsic pathway
hagerman factor - XIIa - XI - IX - VIII - common
absence of factor 12 is the most congenital defect in cats (no clinical bleeding)
common Pathway
X - V - II(prothrombin) - I (fibrinogen) and XIII
thrombin first gets made then that makes fibrinogen
Clotting factor biology
produced in liver.
II, VII, IX, X are vitamin K dependent
VII shortest half life
prevention of uncontrolled clotting
restrict to where it is needed and is restricted to phospholipid surfaces, constant flow of blood dilutes the typical accumulation. (disrupted blood flow could lead to clots)
antithrombin
inhibits thrombin. activated by binding heparin-like molecules (this is why heparin is administered as an anticoagulant)
protein C and S (extended)
Vit. K dependent, inactivate Factors V and VIII, thrombomodulin activates protein C
Plasmin
breaks down fibrin and interferes with polymerization
Fibrin(ogen) degradation products (FDPs)
weak anticoagulant activity
removed by the liver and kidney
primary hemostasis
formation of the primary plug involving blood vessels and platelets
PH characteristics 4
petechiae, ecchymoses, spontaneous bleeding from mucosal surfaces, prolonged bleeding from wounds
PH defects 3
thrombocytopenia (decrease in platelet concentration),
abnormal platelet function (thrombopathy: either vWF disease or taking NSAIDS),
abnormal vasculature
Secondary hemostasis
stabilization of the primary hemostatic plug via the formation of cross linked fibrin by coagulation factors, disorders can be qualitative or quantitative of coagulation factors
What makes most coagulation factors
liver
SH characteristics 4
hematomas, bleeding into cavity, bleeding into muscles and joints, venipuncture later starts to bleed
SH Defects 3
liver disease, congenital absence of clotting factors (hemophilia), Vitamin K deficiency
Vitamin K deficiency
Rodenticide intoxication and moldy sweet clover (cattle)
mixed hemostatic disorders
evidence of primary and secondary hemostasis
Disseminated intravascular coagulation DIC
any type of bleeding with thrombosis.
typically decreased platelets and prolonged clotting time (evidence of increased breakdown of clots)
ALWAYS SECONDARY TO ANOTHER PROCESS
like sepsis, heatstroke, neoplasia
Edema 4
KNOW THIS ONE
increased fluid in interstitial space
low plasma oncotic pressure, increased hydrostatic pressure(impaired venous outflow), lymphatic obstruction, increased vascular permeability
anasarca
generalized SQ edema
ascites
fluid in peritoneal cavity
hydrothorax
fluid in thoracic cavity
hydropericardium
fluid in pericardial sac
hyperemia 5
local increase in blood flow to a tissue with normal to decreased outflow (red, warm, firm)
increased inflow, arteriolar dilation, exercise, inflammation, dissipate heat
congestion 3
local increase in BV due to reduced outflow (red/blue, cool, firm)
Decreased outflow, passive process, pathogenesis related to edema
Types of congestion 5
. Local
b. Pulmonary: inadequate outflow from left heart
c. Systemic: inadequate outflow from right heart
d. Hypostatic congestion: gravitation of blood to dependent regions
e. Post-mortem congestion
ischemia
deprivation of O2 and substrates for glycolysis due to inadequate perfusion (vs. hypoxia alone)
infarction
area of peracute ischemia that undergoes necrosis
if there is anything or moved part that is blocking it is an infarction
thrombosis
formation within a vascular lumen of a thrombus
arterial thrombi
generally endothelial injury and firmly attached to wall
venous thrombi
forms in areas of stasis (due to sluggish blood flow it contains lots of erythrocytes)
there is cardiac thrombi
nothing on it
thrombosis causes 3
endothelial injury, alterations in blood flow (turbulence), hypercoagulability (platelet activation) (coagulation factors)
fate of thrombus 4
propagation or growth (occlusion), embolization, dissolution, organization and recanalization
embolism
detached intravascular matter carried by blood and lodges at a distant site and can cause partial or complete obstructions
shock
- impaired oxygen delivery to the cells due to insufficient cardiac output, loss of
circulating blood volume, or inappropriate peripheral vascular resistance.
cardiogenic shock
myocardial pump failure
hypovolemic shock
blood loss or fluid loss
maldistributive shock
anaphylactic, septic decreased peripheral vascular resistance
obstructive shock
impaired venous return leading to markedly decreased effective circulating volume
Stage 1 of shock: Nonprogressive
blood flow is maintained to certain tissues. have normal readings even though has at least 3 of the 6 main signs
Stage 2 of shock: progressive
BP no longer sustained, pooling of blood and shift to anaerobic resp. lack oxygen and perfusion (hypoxia)
Stage 3 of shock: teriminal
widespread multisystemic injury, ischemia and leading to sepsis, renal failure, DIC
7 clinical signs of Shock
hypotension, weak pulse, tachycardia, decreased urine output, hyperventilation, hypothermia, eventually organ system failure
what to look for with shock 6
Tachycardia, pale MM, higher CRT, cold extremities, poor peripheral pulse, dull mentation
