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Pathology > Circulatory & Hemodynamic disorder > Flashcards

Circulatory & Hemodynamic disorder Flashcards

1
Q

What is edema?

A

H2O shifts from intravascular / intracellular to the interstitial space

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2
Q

What is hyperemia?

A

Active increase in flow

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3
Q

What is congestion?

A

Decreased out flow
Increased venous hydrostatic pressure

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4
Q

What is hemostasis?

A

A physiological response to seal an injured vessel and prevent bleeding

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5
Q

What is thrombosis?

A

Blood clots that blocks blood flow

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6
Q

What is embolus?

A

Abnormal detached traveling intravascular mass

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7
Q

What is infarction?

A

Area of Necrosis after blood flow decreased

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8
Q

What is shock?

A

Cardiovascular collapse / failure of circulation

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9
Q

What is hydrostatic pressure?

A

Hydrostatic pressure is the force created the pumping of the heart that pushes plasma out to interstitial place

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10
Q

Arrange the following by highest hydrostatic pressure to lowest.
Arteries / Capillaries / Veins

A

Arteries > Capillaries > Veins

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11
Q

What is colloid osmotic pressure?

A

Colloid osmotic pressure is the force that holds water in the vessel, mainly by Albumin & sodium

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12
Q

Which factor mainly determines the difference between exudate and transudate?

A

Membrane permeability

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13
Q

Determine if the following factors has to increase or decrease in order to causes edema.
Vascular permeability
Intravascular hydrostatic pressure
Intravascular osmotic pressure
Lymphatic drainage

A

Vascular permeability (I)
Intravascular hydrostatic pressure (I)
Intravascular osmotic pressure (D)
Lymphatic drainage (D)

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14
Q

What is effusions?

A

Increased fluid in body cavities

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15
Q

What is anasarca?

A

Total body edema

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16
Q

What does left and right heart failure cause?

A

Left heart failure : Lung edema
Right heart failure : Ascites

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17
Q

Why causes cardiac edema?
And how to stop it?

A

Left heart failure
-> Lung edema
-> Right heart failure
-> Ascites
-> Reduced blood pressure in arteries
-> Renin - angiotensin

Drugs that promote urine production breaks the cycle of keeping fluid in the body

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18
Q

What causes hepatic edema?

A

Portal hypertension
Hypoalbuminemia : Reduce albumin production

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19
Q

What causes Renal edema?

A

Sodium retention
Glomerulopathy
->Leakage of protein through glomerulus
-> Hypoalbuminemia

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20
Q

Which bacteria could release toxin that destroy endothelial cells and causes exudate?

A

E. coli

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21
Q

What are the 5 types of congestions?

A

Acute local congestion
Chronic local congestion
Acute general congestion
Chronic general congestion
Hypostatic congestion

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22
Q

What causes acute local congestion?

A

Torsion

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23
Q

What happens where spleen had congestion before?

A

Spleen enlargement
Hemosiderin-laden macrophage
Brown induration ( Fibrosis )
Siderotic plaques

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24
Q

What causes chronic local congestion?

A

Tumor, abscess, cirrhosis (Hard liver)

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25
Q

What causes acute general congestion?

A

Acute heart failure
Hydrothorax

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26
Q

What causes chronic general congestion?

A

Chronic heart disease

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27
Q

What happens to Liver after right heart failed?

A

Liver congestion

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28
Q

Explain liver congestion

A

Vena cava congestion causes congestion in central vein

Central vein area receives less O2 than portal triad due to the presence of hepatic artery

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29
Q

What is the difference in lung between acute general congestion and chronic general congestion?

A

Acute general congestion : Lung edema
Chronic general congestion : Hemosiderin-laden macrophages

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30
Q

What are the 3 components for hemostasis?

A

Endothelium & ECM
Platelets
Coagulation factor

31
Q

What are the 3 main groups of coagulative factor?

A

Contact group:
HMWK (High molecular weight kininogen)

Vitamin K dependent group

Fibrinogen group

32
Q

What are the function of endothelium, normal (3) & after injury (2)

A

Normal
-> Anti - platelets
-> Anti - coagulant
-> Pro - fibrinolytic

After injury
-> Pro - thrombotic
-> Anti - fibrinolytic

33
Q

Steps for hemostasis

A

Transient vasoconstriction
-> Reduce blood loss

Platelet aggregation
-> primary hemostasis
(ECM, platelets)

Coagulation to form mesh work of fibrin
-> Secondary hemostasis
(Endothelium, TF, platelets membrane, coagulative factors, Ca++)

Fibrinolysis to remove plug and repair
(Endothelium, Plasminogen -> Plasmin (removes fibrin) -> Thrombomodulin)

34
Q

What are the 3 coagulation inhibitors?

A

Protein C - protein S - thrombomodulin system

Antithrombin lll binds on heparin sulfate

TFPI ( Tissue factor pathway inhibitor )

35
Q

What are the 3 steps in fibrinolytic system?

A

tPA ( Tissue plasminogen activator )
-> Plasminogen => Plasmin

Degradation cross-link fibrin -> FDP ( Fibrin degradation products ) by plasmin

FDP inhibits thrombin & platelet aggregation

36
Q

What are the 2 fibrinolytic inhibitors?

A

PAI -1 ( Plasminogen activator inhibitor -1 )
Antiplasmins

37
Q

What are the 4 disorders of hemostasis?

A

Septicemic disease
Hepatic damage
Vitamin K related
Thrombocytopenia

38
Q

What is the name of vitamin C related hemorrhage? And its mechanisms?

A

Scurvy
X Procollagen => Fibril
-> Weak vessels

39
Q

What is the definition of hematoma?

A

Hemorrhage within organs

40
Q

What is Warfarin poisoning?

A

Excessive amount of anticoagulant medication warfarin

41
Q

Which disease causes cyanosis and hemorrhage in pigs?

A

African swine fever

42
Q

What causes petechial hemorrhage in kidneys ( Turkey egg kidney )?

A

Hog Chloera ( Classical swine fever )

43
Q

Why is arterial thrombus less life threatening than venous thrombus?

A

Arterial thrombus usually develops in the same direction as the blood flow due to the faster blood flow, this means that thrombus will be less likely to block the whole pathway

44
Q

Why is arterial thrombus more pale than venous thrombus?

A

RBC within arteries are less likely to be caught within the thrombus due to faster blood flow

45
Q

What is the line that alternates between fibrin and platelets found in early thrombus?

A

Line of Zahn

46
Q

What mainly causes venous thrombus?

A

Chronic heart failure

47
Q

What are the difference between thrombus and postmortem clotting?

A

Thrombus are attached to the wall of vessels so it is difficult to pull out

48
Q

What is the different fate of small / medium / large thrombi?

A

Small : removed by fibrinolysis
-> plasmin

Medium : removed by phagocytosis

Large : fibroblast invasion + recanalization of capillaries

49
Q

What is DIC?

A

Coagulation in all capillaries

50
Q

Why does animals with DIC loses the ability to coagulate properly when there is a wound?

A

Coagulation factor are used all around the body so they are insufficient amount of them to coagulate properly

51
Q

How to differentiate between DIC & amyloidosis in glomerulus?

A

Congo red staining for amyloid

52
Q

Which of the following is a form of embolism?
Bacterial emboli
Tumor cell emboli
Fat / bone emboli
Air emboli
Parasitic emboli
Amniotic fluid

A

ALL :DDDD
Bacterial : Many many neutrophil
Fat / bone : Long bone fracture ( Cells in bone marrow get into blood after accidents)
Air : Dave the diver ( CO2 becomes air after leaving high pressure area )
Parasitic : Dirofilaria immitis

53
Q

What are the two types of infarcts?

A

Hemorrhage & Anemia

54
Q

What are the difference in color for hemorrhagic infarct & anemic infarct?

A

Red & White

55
Q

Which 2 organs have dual vascular supply?

A

Lung, liver

56
Q

Match the correct organ ( Lungs / Spleen / Kidney ) into ( Red infarct / White infarct ) and explain why.

A

Red infarct : Lung
White infarct : Spleen / Kidney

Lung has rich blood supply so when a vessel is blocked, blood supply is not completely cut off. However, blood will continue to enter the infarcted tissue ( Hemorrhage ) can causes a red appearance -> Red infarct

Spleen and kidney has a single dominant blood supply ( End arteries ), and if it is blocked, the lack of oxygenated blood -> White infarct

57
Q

What 4 organs have end arteries?

A

Kidney, spleen, heart, brain

58
Q

What are the 2 causes for red infarcts due to venous obstruction

A

Mass : Tumor, abscess
Torsion

59
Q

What is the 2 similarities of splenic infarct and renal infarct?

A

End arteries obstruction
Triangular shape necrosis

60
Q

Which parasite causes intestinal infarct?

A

Strongylus

61
Q

What happens when cardiovascular collapse?

A

Shock
-> Systemic hypoperfusion of tissue

62
Q

Which of the following are the causes of shock?
Hypovolemic
Cardiac
Septic & Toxic
Neurogenic
Anaphylatic

A

Hypovolemic : Vomiting, diarrhea

Cardiac : Chronic heart failure
(Both hypovolemic & cardiac : Lowered output)

Septic & Toxic : LPS, DIC

Neurogenic : Loss of vascular tone

Anaphylactic : IgE mediated vasodilation

63
Q

What are the name of the two shock stages?

A

Non progressive / Compensated stage

Progressive stage

64
Q

What are the mechanisms in compensated shock stage?

A

Release of catecholamines ( Sympathetic )

Activation of renin - angiotensin - aldosterone axis

-> Lower cardiac output -> Compensation from body ( Increase blood pressure, increase heart rate )

65
Q

What are the effects from the mechanisms in compensated shock stage?

A

Tachycardia

Peripheral vasoconstriction

Cutaneous vasoconstriction
-> Pale skin color and cold skin

Renal fluid conservation

66
Q

What happens in our body during progressive stage?

A

Tissue hypoperfusion
-> Hypoxia
—>Metabolic lactic acidosis
—–> Clumping of DNA
—–> Organelle damage
—–> Sudden vasodilation of capillaries
——-> Cardiac output (D even more)

67
Q

What happens when irreversible shock stage?

A

Dead even hemodynamic defects are corrected

68
Q

What are the order of shock?
Progressive, compensated, normal, irreversible

A

Normal > Compensated > Progressive > Irreversible

69
Q

What happens with cardiac output in different shock stages?

A

Compensated (High)
Progressive (D)
Irreversible (byebye)

70
Q

What happens with cardiac rate in different shock stages?

A

Compensated (High)
Progressive (High)
Irreversible (byebye)

71
Q

What happens with vital perfusion in different shock stages?

A

Compensated (Normal)
Progressive (Normal)
Irreversible (byebye)

72
Q

What happens with non vital perfusion in different shock stages?

A

Compensated (D)
Progressive (D)
Irreversible (byebye)

73
Q

What happens with oxidative - phosphorylation in different shock stages?

A

Compensated ( Normal (high) )
Progressive (D)
Irreversible (byebye)

74
Q

What happens with glycolysis in different shock stages?

A

Compensated ( Normal (low) )
Progressive (I)
Irreversible (byebye)

Pathology (5 decks)

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