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Basic Pathology > Friedenberg and Lab Basic Pathology > Flashcards

Friedenberg and Lab Basic Pathology Flashcards

1
Q

Clinical diagnosis

A

from case history, clinical signs, and physical exam

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2
Q

etiology

A

cause of disease

can be intrinsic or extrinsic and be as specific as possible

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3
Q

differential diagnoses

A

lost of diagnoses that could account for the clinical signs or lesions

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4
Q

Components of morphological diagnosis

A

organ, process, process modifier, distribution, (duration, severity)

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5
Q

Most Likely diagnosis

A

greatest possibility based on the available evidence

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6
Q

description of pathological lesions

A

Visual, palpable, incision

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7
Q

Differentiation of tissue

A

lesion, postmortem artifact, variation of normal

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8
Q

focal

A

one location

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9
Q

multifocal

A

a few singular spots around

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10
Q

multifocal coalescing

A

spots around and some are close and forming together

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11
Q

widely disseminated

A

lots of spots all over the organ or tissue

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12
Q

locally extensive

A

clump of a lot in one area

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13
Q

diffuse

A

completely covered

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14
Q

segmental

A

large chunk one piece around cylinder

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15
Q

annular

A

small band around it cylinder

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16
Q

transmural

A

different lesions different ways when tube is cut

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17
Q

-itis

A

inflammation

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18
Q

4 major processes

A

degenerative/necrosis, inflammation/repair, circulatory disturbances, growth disturbances

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19
Q

sarcoma

A

malignant tumor of mesenchymal cell organs (muscle, bones, vascular)

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20
Q

Carcinoma

A

epithelial cells of the organs

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21
Q

fibroma

A

benign tumor of fibroblast

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22
Q

osteosarcoma

A

malignant tumor of osteoblasts

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23
Q

hepatocellular carcinoma

A

malignant tumor of hepatocytes

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24
Q

thrombosis

A

excessive coagulation (clotting) in blood

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25
Q

hemorrhage

A

deficient coagulation (clotting) in the blood

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26
Q

hemostasis 3

A

blood vessel wall, platelets, coagulation factors

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27
Q

Normal homeostasis

A

endothelium of vessels antagonize clot formation through:

vasodilation, inhibit platelet adhesion, aggregation, inhibit coagulation

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28
Q

Vascular injury 5 steps

A

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

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29
Q

endothelium

A

antagonize or stimulate coagulation (the balance of this determines the physiological outcome)
either anticoagulant or procoagulant

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30
Q

Nitric oxide and prostacyclin PGI2

A

maintain vascular relaxation and inhibit adnesion and aggregation of platelets

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31
Q

adenosine-diphosphatase

A

an enzyme that degrades ADP (a stimulation of platelet aggregation)

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32
Q

Membrane associated heparin-like anticoagulants

A

potentiates the activity of antithrombin

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33
Q

antithrombin

A

potent anticoagulant

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34
Q

thrombomodulin

A

bonds to thrombin and converts it from a procoagulant to anticoagulant that activates protein C

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35
Q

protein C and S

A

vitamin K dependent factors that degrade coagulation factors

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36
Q

tissue plasminogen activator (t-PA)

A

promotes fibrinolysis

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37
Q

tissue factor pathway inhibitor (TFPI)

A

inactivates tissue factor VIIa complexes

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38
Q

von willibrand factor (vWF)

A

mediates platelet binding to subendothelial collagen and other surfaces

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39
Q

Tissue factor (Factor III)

A

initiates the coagulation cascade

40
Q

Plasminogen activator inhibitors (PAIs)

A

inhibit fibrinolysis

41
Q

Platelets forming primary hemostatic plug 4

A

adhesion, secretion, activation, aggregation

42
Q

adhesion

A

platelets interact with vWF and creates a bridge between subendothelial ECM and platelet surface receptors

43
Q

secretion

A

secrete alpha granules and dense bodies (release Ca that starts coag. cascade) and ADP to mediate Aggregation

44
Q

activaton

A

expression of phospholipid complex on surface of platelets for Ca and coag. factor binding

45
Q

aggregation

A

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)

46
Q

fibrinogen

A

links activated platelets to form large platelet aggregates with a receptor. the receptor is necessary or they could develop a bleeding disorder

47
Q

platelet functions

A

wound healing, angiogenesis, metastasis of neoplasia

48
Q

coagulation cascade

A

intrinsic and extrinsic pathways that converge to the common pathway

49
Q

Initiation of coagulation

A

primarily through tissue factor activation of the extrinsic pathway

50
Q

end result of coagulation cascade

A

thrombin and fibrinogen to fibrin (cross linked) forming a plug

51
Q

Cell-based model

A

not what we use but is the more accurate coagulation cascade

52
Q

extrinsic pathway

A

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)

53
Q

intrinsic pathway

A

hagerman factor - XIIa - XI - IX - VIII - common

absence of factor 12 is the most congenital defect in cats (no clinical bleeding)

54
Q

common Pathway

A

X - V - II(prothrombin) - I (fibrinogen) and XIII

thrombin first gets made then that makes fibrinogen

55
Q

Clotting factor biology

A

produced in liver.
II, VII, IX, X are vitamin K dependent

VII shortest half life

56
Q

prevention of uncontrolled clotting

A

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)

57
Q

antithrombin

A

inhibits thrombin. activated by binding heparin-like molecules (this is why heparin is administered as an anticoagulant)

58
Q

protein C and S (extended)

A

Vit. K dependent, inactivate Factors V and VIII, thrombomodulin activates protein C

59
Q

Plasmin

A

breaks down fibrin and interferes with polymerization

60
Q

Fibrin(ogen) degradation products (FDPs)

A

weak anticoagulant activity

removed by the liver and kidney

61
Q

primary hemostasis

A

formation of the primary plug involving blood vessels and platelets

62
Q

PH characteristics 4

A

petechiae, ecchymoses, spontaneous bleeding from mucosal surfaces, prolonged bleeding from wounds

63
Q

PH defects 3

A

thrombocytopenia (decrease in platelet concentration),
abnormal platelet function (thrombopathy: either vWF disease or taking NSAIDS),
abnormal vasculature

64
Q

Secondary hemostasis

A

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

65
Q

What makes most coagulation factors

A

liver

66
Q

SH characteristics 4

A

hematomas, bleeding into cavity, bleeding into muscles and joints, venipuncture later starts to bleed

67
Q

SH Defects 3

A

liver disease, congenital absence of clotting factors (hemophilia), Vitamin K deficiency

68
Q

Vitamin K deficiency

A

Rodenticide intoxication and moldy sweet clover (cattle)

69
Q

mixed hemostatic disorders

A

evidence of primary and secondary hemostasis

70
Q

Disseminated intravascular coagulation DIC

A

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

71
Q

Edema 4

KNOW THIS ONE

A

increased fluid in interstitial space
low plasma oncotic pressure, increased hydrostatic pressure(impaired venous outflow), lymphatic obstruction, increased vascular permeability

72
Q

anasarca

A

generalized SQ edema

73
Q

ascites

A

fluid in peritoneal cavity

74
Q

hydrothorax

A

fluid in thoracic cavity

75
Q

hydropericardium

A

fluid in pericardial sac

76
Q

hyperemia 5

A

local increase in blood flow to a tissue with normal to decreased outflow (red, warm, firm)
increased inflow, arteriolar dilation, exercise, inflammation, dissipate heat

77
Q

congestion 3

A

local increase in BV due to reduced outflow (red/blue, cool, firm)
Decreased outflow, passive process, pathogenesis related to edema

78
Q

Types of congestion 5

A

. 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

79
Q

ischemia

A

deprivation of O2 and substrates for glycolysis due to inadequate perfusion (vs. hypoxia alone)

80
Q

infarction

A

area of peracute ischemia that undergoes necrosis

if there is anything or moved part that is blocking it is an infarction

81
Q

thrombosis

A

formation within a vascular lumen of a thrombus

82
Q

arterial thrombi

A

generally endothelial injury and firmly attached to wall

83
Q

venous thrombi

A

forms in areas of stasis (due to sluggish blood flow it contains lots of erythrocytes)

84
Q

there is cardiac thrombi

A

nothing on it

85
Q

thrombosis causes 3

A

endothelial injury, alterations in blood flow (turbulence), hypercoagulability (platelet activation) (coagulation factors)

86
Q

fate of thrombus 4

A

propagation or growth (occlusion), embolization, dissolution, organization and recanalization

87
Q

embolism

A

detached intravascular matter carried by blood and lodges at a distant site and can cause partial or complete obstructions

88
Q

shock

A
  • impaired oxygen delivery to the cells due to insufficient cardiac output, loss of
    circulating blood volume, or inappropriate peripheral vascular resistance.
89
Q

cardiogenic shock

A

myocardial pump failure

90
Q

hypovolemic shock

A

blood loss or fluid loss

91
Q

maldistributive shock

A

anaphylactic, septic decreased peripheral vascular resistance

92
Q

obstructive shock

A

impaired venous return leading to markedly decreased effective circulating volume

93
Q

Stage 1 of shock: Nonprogressive

A

blood flow is maintained to certain tissues. have normal readings even though has at least 3 of the 6 main signs

94
Q

Stage 2 of shock: progressive

A

BP no longer sustained, pooling of blood and shift to anaerobic resp. lack oxygen and perfusion (hypoxia)

95
Q

Stage 3 of shock: teriminal

A

widespread multisystemic injury, ischemia and leading to sepsis, renal failure, DIC

96
Q

7 clinical signs of Shock

A

hypotension, weak pulse, tachycardia, decreased urine output, hyperventilation, hypothermia, eventually organ system failure

97
Q

what to look for with shock 6

A

Tachycardia, pale MM, higher CRT, cold extremities, poor peripheral pulse, dull mentation

Basic Pathology (4 decks)

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