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Pathology I Test I > Hemodynamic disorders > Flashcards

Hemodynamic disorders Flashcards

1
Q

What are two types of edema?

A

Exudate and Transudate

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2
Q

What is exudate made of?

A

It is rich in protein and blood cells and are typical of inflammation

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3
Q

What is transudate made of?

A
  • Contains less protein and fewer cells

- an ultra-filtrate of plasma fluid

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4
Q

What is a typical cause of transudate?

A

Typical of hydrostatic or osmotic pressure pathology

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5
Q

What is the specific gravity of transudate?

A

Specific gravity is usually less than 1.012 and a protein content of less than 2gm/100mL

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6
Q

What are some factors towards the pathogenesis of Edema?

A

1) increase in hydrostatic pressure
2) Increase in wall permeability
3) Decrease oncotic pressure (decrease albumin concentration)
4) Lymphatic obstruction

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7
Q

Is transudate hypocellular or cellular?

A

Hypocellular

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8
Q

Is transudate protein rich or poor?

A

Protein poor

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9
Q

What is the specific gravity of transudate?

A

Specific gravity <1.012

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10
Q

What is transudate due to?

A

Increased hydrostatic pressure
Decreased Oncotic pressure
Na+ retention

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11
Q

Is exudate hypocellular or cellular?

A

Cellular

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12
Q

Is exudate protein rich or poor?

A

Protein rich

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13
Q

What is the specific gravity of exudate?

A

Specific gravity >1.020

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14
Q

What is exudate due to?

A

Lymphatic obstruction

Inflammation

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15
Q

What Is the different types of pathogenesis causes of Edema?

A

1) Inflammatory
2) Hydrostatic
3) Oncotic
4) Obstructive
5) Hypervolemic

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16
Q

Why does inflammatory lead to the pathogenesis of edema?

A

Increases permeability & hyperemia

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17
Q

How does hydrostatic lead to the pathogenesis of edema?

A

Increased arterial pressure (hypertension)

Increased venous back pressure (heart failure)

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18
Q

How does the oncotic pressure lead to the pathogenesis of edema?

A

Hypoalbuminemia due to:

  • loss/proteinuria
  • decreased protein synthesis
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19
Q

How does the obstruction lead to the pathogenesis of edema?

A
  • Most often b tumor or chronic inflammation

- Filaria (worm) -> elephantiasis

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20
Q

How does hypovolemia lead to the pathogenesis of edema?

A

Usually d/t sodium and water retention:

  • kidney function, renin, angiotensinogen, & aldosterone
  • Kidney disease -> increased renin release -> angiotensinogen -> increased aldosterone -> increased Na retention -> increased water retention
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21
Q

What are some clinical forms of edema?

A

1) Cerebral edema
2) Pulmonary edema (d/t left-sided heart failure, post-surgery)
3) Pitting edema of the lower extremities
4) Periorbital (facial) edema
5) Hydrothroax
6) Hydropericardium
7) Hydroperitoneum (ascites)
8) Anasarca (Extremegeneralized edema)

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22
Q

What are some clinical correlations of edema in regards to the heart?

A
  • edema of lower extremities
  • edema of back if pt is supine
  • left ventricular failure - pulmonary effects
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23
Q

What are some clinical correlations of edema in regards to the kidneys?

A
  • typically diffuse

- renal failure or nephrotic syndrome

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24
Q

What are some clinical correlations of edema in regards to the liver?

A
  • ascites d/t low albumin & portal hypertension
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25
Q

What is active hyperemia?

A

Dilatation of arterioles leading to blushing, exercise, inflammation

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26
Q

What is passive hyperemia?

A

Venous back pressure; often associated with hydrostatic edema, cyanosis
- heart failure - pulmonary edema and heart failure cells

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27
Q

What does a chronic passive congestion of lungs lead to?

A

Leads to edema and RBC extravasation into alveoli

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28
Q

What is a chronic passive congestion of lungs accompanied by?

A

Accompanied by anoxia & often results in pulmonary fibrosis

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29
Q

In a chronic passive congestion of the lungs, what does an alveolar macrophage do?

A

Alveolar macrophages take up RBC & degrade hemoglobin = hemosiderin accumulation

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30
Q

Cardiac hemorrhage is often what? And what is it caused by?

A
  • often fatal

- MI, Gun Shot Wound, stabbing wound

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31
Q

What is an aortic hemorrhage caused by?

A
  • MVA (organs kee moving at a high speed and rips off part of aorta via ligamentum arteriosum
  • weakness due to copper deficiency -> aneurysm
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32
Q

What will an arterial hemorrhage look like? What causes it?

A
  • penetrating wound, fractured bones

- presents as a bright red, pulsating/squirting

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33
Q

What will cause a capillary hemorrage? What does it do to venous pressure?

A
  • Trauma, weakness due to vitamin C (scurvy) -increase in venous pressure
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34
Q

With the venous, how does it present as a hemorrhage?

A

Dark/bluish color, oozing

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35
Q

In a hemorrage what are some signs and symptoms?

A
  • Intracerebral hemorrhage
  • Hematemesis or hemoptysis
  • Cardiac hemorrhage
  • Venous hemorrhage
  • Aortic hemorrhage
  • Capillary hemorrhage
  • hematochezia or melena (from anus)
  • Hematuria
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36
Q

What are some clinically important forms of hemorrhage?

A
  • skin/surface hemorrhage
  • large accumulation of blood in body cavities/space
  • hemoptysis
  • epistaxis
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37
Q

What are some different types of skin/surface hemorrhage?

A
  • petechia
  • purpura
  • ecchymosis
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38
Q

What is a petechia?

A

<1 mm and speckles of blood vessels

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39
Q

What is purpura?

A

Between 1 mm- 1cm and larger blotches

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40
Q

What is ecchymosis?

A

Large/blotchy bruises

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41
Q

What are some large accumulation of blood in body cavities/spaces?

A

Hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis

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42
Q

What is a hemoptysis?

A

Respiratory tract/expectoration of blood

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43
Q

What is a epistaxis?

A

Nose bleed

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44
Q

What is hematemesis?

A

Vomiting blood

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45
Q

What is hematochezia

A

anorectal bleeding

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46
Q

what is melena

A

passage of black blood in stool

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47
Q

what is hematuria

A

blood in urine

48
Q

What is metrorrhagia?

A

bleeding not related to normal monthly menses

49
Q

what is menorrhagia?

A

Profound menstrual bleeding

50
Q

What happens in a massive hemorrhage?

A

Blood loss, hypovolemic shock, exsanguination, death

51
Q

If <500 ml of blood is lost what happens?

A

homeostatic compensation but it is reversible

52
Q

If 1000-1500 ml of blood is lost what happens?

A

Circulatory shock

53
Q

If >1500 ml of blood is lost what happens?

A

Lethal

54
Q

What are some of the types of hemorrhage?

A
  • Massive hemmorhage
  • Hematoma
  • Intracerebral hemorrhage
  • Chronic hemorrhage
55
Q

What can an intracerebral hemorrhage lead to?

A

Stroke, death

56
Q

What can a chronic hemorrhage lead to?

A

Slow blood loss, iron deficiency anemia (70 ml for normal menstruation)

57
Q

Which hemorrhage has a better outcome, Subdural or epidural hemorrhage?

A

A subdural hemorrhage because the lower pressure veins bleed more slowly than arteries

58
Q

What is a thrombosis?

A

clotting due to a transformation of the fluid blood into a solid aggregate encompassing RBCs and fibrin

59
Q

Women smokers who use oral contraceptives have a serious risk for what?

A

Consequences including increased risk of developing cardiovascular diseases such as blood clots, heart attacks and strokes

60
Q

What are three principal components of intravascular coagulation?

A

1) Coagulation factors
2) Platelets
3) Endothelial cells

61
Q

What are coagulation factors?

A

Endogenous (intrinsic) and/or exogenous (extrinsic) pathways

62
Q

What are platelets?

A
  • Neutralize heparin & other anticoagulant factors

- secrete thromboxane - stimulate coagulation process

63
Q

What properties do endothelial cells have and what normally activates them?

A

Normally endothelial cells have antithrombotic properties that are activated by IL-1 & TNF which causes them to lose their negative charge and antithrombotic

64
Q

Name the 3 body fluid compartments?

A

intracellular, interstitial, intravascular.

65
Q

How much fluid is taken in a day?

A

2.5 liters.

66
Q

How much fluiid 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.

67
Q

Elephantiasis is caused by what?

A

Lymph blockage from a parasite.

68
Q

Skin hemorrhages are what?

A

Bruises

69
Q

What is the first step in forming a thrombi?

A

Defect is covered with fibrin and platlets.

70
Q

What is the second step in forming a thrombi?

A

Fibrin meshwork anchors RBCs into nascent thrombus.

71
Q

What is the third step in forming a thrombi?

A

Fully formed thrombi consists of layers of fibrin and RBCs

72
Q

Intramural thrombi of the heart causes what?

A

overlying Myocardial infarct.

73
Q

Valvular thrombi of the heart causes what?

A

mimic endocarditis.

74
Q

arterial thrombi cause what?

A

atherosclerosis when attached to the walls. Can be found with aortic aneurysms

75
Q

When is a venous thrombi found?

A

in dialated veins. (varicose veins)

76
Q

Where are microvascular thrombi found at?

A

Arterioles, capillaries, and venules.

77
Q

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

A
  1. Stasis.
  2. Hypercoagulability.
  3. endothelial damage.
78
Q

Who is at risk for deep venous thrombosis?

A

Elderly people on transcontinental flights and birth control pills and smoking

79
Q

What are lines of zahn?

A

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

80
Q

Occlusion of the lumen from a thrombi is called what?

A

Infarct.

81
Q

Lysis of the thrombus is called?

A

reperfusion.

82
Q

Recanalization of a thrombus leads to what?

A

reestablished blood flow.

83
Q

What is embolization of a thrombi?

A

Breaking off of a clot.

84
Q

What are the five different fates for thrombi?

A

1) Occlusion of the lumen
2) Lysis of the thrombus
3) Organization of the thrombus (find another route)
4) Recanalization
5) Embolization

85
Q

What is an embolus?

A

Undissolved materials like thrombus in blood.

86
Q

Name 4 types of embolisms?

A

1) thromboemboli
2) liquid emboli
3) gaseous emboli
4) solid particle emboli.

87
Q

Amniotic fluid emboli can lead to what?

A

DIC (disseminated intravascular coagulation), especially postpartum.

88
Q

What can cause liquid emboli?

A

Fat (long bone fracture), oil, amniotic fluid

89
Q

What can cause gaseous emboli?

A

Aire injection, caisson disease (decompression sickness from N2)

90
Q

What can cause solid particle emboli?

A

Cholesterol crystals (atheromatous plaques), bone marrow (fractures), tumor emboli (most common solid particle emboli)

91
Q

Pulmonary embolus clinically present with what?

A

Chest pain, tachypnea, dyspnea.

92
Q

95% of pulmonary emboli arise from what?

A

Deep leg veins.

93
Q

What are the origins of venous thromboemboli?

A

Anywhere (but on diagram it is saddle, lung, venous thrombi.)

94
Q

What are the origins of arterial thromboemboli?

A

Cerebral infarcts
Left ventricle
(on diagram it is: brain, kidney, spleen, Intestinal, ventricular and extremity infarct.)

95
Q

A white infarct is typical of what?

A

`Arterial occlusion in solid organs with single blood supply. (ie: heart, kidney, spleen)

96
Q

Red infarct is typical of what?

A

Venous obstruction like intestines and testes twisting.

97
Q

The fate of infarcts depends on what?

A

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

98
Q

What areas do white infarcts occur on organs?

A

Rimmed areas

99
Q

What is a volvulus?

A

Twisting

100
Q

What type of infarct is seen with volvulus?

A

Red infarct

101
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.
102
Q

Pump failure leads to what type of shock?

A

Cardiogenic shock.

103
Q

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

A

Hypovolemic shock.

104
Q

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

A

Hypotensive shock.

105
Q

Loss of blood, myocardial or valvular disease, or vasodilation leads to what?

A

Heart failure

106
Q

heart failure leads to what?

A

Decreased cardiac output.

107
Q

Decreased cardiac output leads to what?

A

Decreased blood to tissues.

108
Q

Decreased blood to tissues leads to what?

A

Cell anoxia.

109
Q

Cell anoxia leads to what?

A

Shock and edema

110
Q

Shock leads to what?

A

Coma, renal failure, lung failure, death, gi bleeding.

111
Q

What are the 3 clinical stages of shock?

A
  1. early or compensated shock.
  2. Decompensated but reversible shock.
  3. Irreversible shock.
112
Q

What happens with the heart during compensated shock?

A

Tachycardia (beats faster). (D/t CO = SV X HR, low SV means higher HR to compensate)

113
Q

Besides heart compensation, what else happens with compensated shock?

A

Vasoconstriction of arterioles and reduced urine production.

114
Q

What happens with decompensated reversible shock?

A

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

115
Q

What happens with irreversible shock?

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

Pathology I Test I (5 decks)

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