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Pathology 1 > Ch 4 - Hemodynamic disorders > Flashcards

Ch 4 - Hemodynamic disorders Flashcards

1
Q

Name the 3 body fluid compartments?

A

intracellular, interstitial, intravascular.

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2
Q

How much fluid is taken in a day?

A

2.5 liters.

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3
Q

How much fluid is let out in a day and how?

A

2.5 liters. 0.1 in stool, 0.9 in respiration/sweat, 1.5 in urine.

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4
Q

What are the 2 forms of edema?

A
  1. Exudate. 2. Transudate.
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5
Q

Which type of edema is typical of inflammation?

A

Exudate.

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6
Q

What is exudate rich in?

A

Protein and blood cells.

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7
Q

Transudate contains less proteins and fewer cells and is typical of what?

A

Hydrostatic or osmotic pressure pathology.

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8
Q

What is transudate?

A

An ultra-filtrate of plasma fluid.

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9
Q

4 factors of pathogenesis of edema?

A
  1. Increased hydrostatic pressure. 2. Increased wall permeability. 3. decreased oncotic pressure. 4. Lymphatic obstruction.
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10
Q

What is hydrostatic pressure?

A

Blood pressure pushing fluid OUT of capillaries.

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11
Q

What is oncotic pressure?

A

Plasma proteins that are in capillaries want to be diluted - pull fluid back INTO the capillary.

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12
Q

Transudate vs exudate - hypocellular/cellular?

A

Transudate - hypocellular Exudate - cellular

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13
Q

Transudate vs exudate - protein rich?

A

Transudate - protein POOR Exudate - protein RICH

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14
Q

Transudate edema - specific gravity higher or lower than 1.012?

A

Lower.

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15
Q

Exudate edema - specific gravity higher or lower than 1.020?

A

Higher

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16
Q

What causes transudate edema?

A

Increased hydrostatic pressure, incresed oncotic pressure, Na retention.

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17
Q

What causes exudate edema?

A

Lymphatic obstruction, INFLAMMATION

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18
Q

Hydrostatic pressure causes edema and is caused by what 2 things?

A

hypertension (increased arterial pressure), heart failure (increased venous backpressure).

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19
Q

Oncotic pressure, when low, causes edema and is caused by what?

A

decreased protein synthesis, proteinuria (loss of proteins in urine).

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20
Q

Obstructions that cause edema are usually caused by what?

A

Tumors or chronic inflammation, also parasites like filaria which causes elephantiasis.

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21
Q

What is hypervolemic?

A

High levels of blood.

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22
Q

Hypervolemia causes edema - what causes it?

A

Na and H2O retention.

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23
Q

What is anasarca?

A

Extreme generalized edema.

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24
Q

What are hydrothorax, hydropericardium, and hydroperitoneum?

A

Clincal forms of edema that are in cavities.

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25
Q

Low blood pressure leads to what type of edema?

A

Pulmonary edema (left sided heart failure)

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26
Q

Elephantiasis is caused by what?

A

Lymph blockage from a parasite.

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27
Q

Heart problems will show edema where?

A

lower extremities, or back if patient supine.

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28
Q

Kidney problems will show edema where?

A

Diffuse edema.

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29
Q

Liver problems will show edema where?

A

ascites (fluid in peritoneal cavity) due to low albumin and portal hypertension.

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30
Q

What is hyperemia?

A

Excess blood flow.

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31
Q

What is active hyperemia?

A

Dialation of arterioles like when blushing, exercise, inflammation.

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32
Q

What is passive hyperemia?

A

Venous backpressure

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33
Q

What is passive hyperemia associated with?

A

hydrosatic edema, cyanosis, and heart failure.

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34
Q

What does chronic passive congestion of lungs lead to?

A

edema and RBC extravasation into alveoli.

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35
Q

What is chronic passive congestion of the lungs accompanied by?

A

Anoxia (low oxygen in blood), and pulmonary fibrosis.

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36
Q

With chronic passive congestion of the lungs, macrophages take up RBCs and degrade hemoglobin - what does this lead to?

A

Hemosiderin accumulation.

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37
Q

Cardiac hemorrhage is often what?

A

Fatal.

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38
Q

What will arterial hemorrhage look like?

A

Bright red pulsating/squirting.

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39
Q

Capillary hemorrhage does what to venous pressure?

A

increases it.

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40
Q

What does venous hemorrhage look like?

A

Dark/bluish color, oozing

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41
Q

What are skin hemorrhages?

A

Bruises

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42
Q

What is a purpura?

A

A skin hemorrhage that is between 1mm and 1 cm.

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43
Q

What is ecchymosis?

A

A skin hemorrhage - large blotchy bruises

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44
Q

What is petechia?

A

Skin hemorrhages that are less than 1mm.

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45
Q

What is hemoptysis?

A

Respiratory tract hemorrhage - coughing up blood

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46
Q

What is epistaxis?

A

Nose bleeds.

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47
Q

What is hematemesis?

A

Vomiting blood.

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48
Q

What is hematochezia?

A

Anorectal bleeding.

49
Q

What is melena?

A

Passage of black blood in stool from bleed in upper GI tract.

50
Q

What is hematuria?

A

Blood in urine.

51
Q

What is metrorrhagia?

A

Bleeding not related to normal monthly menses.

52
Q

What is menorrhagia?

A

Profound menstrual bleeding.

53
Q

How much blood can we lose and be ok?

A

Less than 500 ml

54
Q

What happens if we lose 1000- 1500 ml of blood?

A

Circulatory shock.

55
Q

How much blood loss is lethal?

A

1500 ml or more.

56
Q

What is hematoma?

A

Compression of tissues.

57
Q

What happens with intracerebral hemorrhage?

A

Stroke, death.

58
Q

Slow chronic hemorrhage leads to what?

A

Iron deficiency anemia.

59
Q

What type of hemorrhage has slower onset - subdural or epidural? And why?

A

Subdural - the lower pressure veins bleed more slowly than arteries.

60
Q

What is thrombosis?

A

Clotting.

61
Q

How does thrombosis take place?

A

transformation of fluid blood into a solid aggregate encompassing RBCs and fibrin.

62
Q

What does thrombosis form?

A

A thrombus.

63
Q

What are the 3 principle components of an intravascular coagulation?

A
  1. Coagulation factors. 2. Platelets. 3. Endothelial cells.
64
Q

What are the 2 pathways for coagulation factors?

A

Endogenous (intrinsic) and exogenous (extrinsic).

65
Q

What 2 things will platelets do?

A
  1. neutralize heparin and other anticoagulant factors 2. secrete thromboxane, which stimulates coagulation.
66
Q

What do endothelial cells normally have?

A

Antithrombotic properties.

67
Q

What happens when IL-1 and TNF activate endothelial cells?

A

They lose their negative charge and antithrombotic properties

68
Q

Endothelial damage uses which coagulation factor pathway?

A

Intrinsic.

69
Q

Tissue damage uses which coagulation factor pathway?

A

Extrinsic.

70
Q

What is the first step in forming a thrombi?

A

Defect is covered with fibrin and platlets.

71
Q

What is the second step in forming a thrombi?

A

Fibrin meshwork anchors RBCs into nascent thrombus.

72
Q

What is the third step in forming a thrombi?

A

Fully formed thrombi consists of layers of fibrin and RBCs

73
Q

What does intramural thrombi of the heart cause?

A

overlying Myocardial infarct.

74
Q

What does valvular thrombi of the heart mimic?

A

endocarditis (small fibrinous excretions).

75
Q

What do arterial thrombi cause?

A

atherosclerosis when attached to the walls, can be found in aortic aneurysms

76
Q

Where is a venous thrombi found?

A

in dilated veins (vericose veins)

77
Q

Where are microvascular thrombi found at?

A

Arterioles, capillaries, and venules.

78
Q

How are thrombi classified?

A

On the basis of their location

79
Q

What can deep venous thrombosis lead to?

A

Pulmonary embolism

80
Q

Deep venous thrombosis is predisposed by Virchow’s triad, which is what 3 things?

A
  1. Stasis. 2. Hypercoagulability (inflammation, increased ESR) 3. endothelial damage.
81
Q

Who is at risk for deep venous thrombosis?

A

Elderly people on transcontinental flights.

82
Q

What are lines of zahn?

A

Distinct layering of cellular elements and fibrin that occur in atrial and venous thrombi.

83
Q

What is occlusion of the lumen from a thrombi called?

A

Infarct.

84
Q

What is lysis of the thrombus called?

A

reperfusion.

85
Q

What does recanalization of the thrombus do?

A

reestablish blood flow

86
Q

What is embolization of a thrombi?

A

Breaking off of a clot.

87
Q

What is an embolus?

A

Undissolved materials like thrombus in blood.

88
Q

Name 4 types of embolisms?

A

thromboemboli, liquid emboli, gaseous emboli, solid particle emboli.

89
Q

What is the most common etiology for an embolism?

A

Thromboemboli

90
Q

What can cause a liquid embolism?

A

oil, fat (long bone fracture), amniotic fluid

91
Q

What can cause a gaseous embolism?

A

Air injection, caisson disease (decompression sickness, from N2)

92
Q

What can cause a solid particle embolism?

A

cholesterol crystals, bone marrow (from fractures), tumor emboli

93
Q

What can amniotic fluid emboli lead to?

A

DIC, especially postpartum.

94
Q

What does pulmonary embolus clinically present with?

A

Chest pain, tachypnea, dyspnea.

95
Q

95% of pulmonary emboli arise from what?

A

Deep leg veins.

96
Q

Origin of venous thromboemboli?

A

Anywhere

97
Q

Origin of arterial thromboemboli?

A

Left ventricle

98
Q

What is white infarct typical of?

A

Arterial occlusion in solid organs with single blood supply (heart, kidney, spleen)

99
Q

What is red infarct typical of?

A

Venous obstruction, like intestines and testis twisting.

100
Q

What does the fate of infarcts depend on?

A

Their anatomical site, type of cells forming the tissue, circulatory status , extent of necrosis.

101
Q

White infarcts are ________ areas.

A

Rimmed

102
Q

What is volvulus?

A

Twisting.

103
Q

What type of infarct is seen with volvulus?

A

Red infarct.

104
Q

What are 3 possible causes of shock?

A
  1. Pump failure of the heart. 2. Loss of fluid from circulation. 3. Loss of peripheral vascular tone.
105
Q

Pump failure leads to what type of shock?

A

Cardiogenic shock.

106
Q

Loss of fluid from circulation lead to what type of shock?

A

Hypovolemic shock.

107
Q

Loss of peripheral vascular tone leads to what type of shock?

A

Hypotensive shock.

108
Q

What will loss of blood, myocardial or valvular disease, or vasodilation lead to?

A

Heart failure

109
Q

What does heart failure lead to?

A

Decreased cardiac output.

110
Q

What will decreased cardiac output lead to?

A

Decreased blood to tissues (hypoperfusion)

111
Q

What will hypoperfusion lead to?

A

Cell anoxia.

112
Q

What will cell anoxia lead to?

A

Shock and edema

113
Q

What does shock lead to?

A

Coma, renal failure, lung failure, GI bleeding, death

114
Q

What are the 3 clinical stages of shock?

A
  1. early or compensated shock. 2. Decompensated but reversible shock. 3. Irreversible shock.
115
Q

What happens with the heart during compensated shock?

A

Tachycardia (beats faster).

116
Q

What happens to arterioles during compensated shock?

A

Vasoconstriction - vital organ perfusion

117
Q

What happens to urine production during compensated shock?

A

Reduced urine production

118
Q

What happens with decompensated reversible shock?

A

hypotension, tachypnea and shortness of breath, oliuria, acidosis.

119
Q

What happens with irreversible shock?

A
  1. Circulatory collapse. 2. marked hypoperfusion of vital organs. 3. Loss of vital functions.

Pathology 1 (6 decks)

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