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Pathology > Edema, Hemorrhage, Congestion and Shock > Flashcards

Edema, Hemorrhage, Congestion and Shock Flashcards

1
Q

edema

A

increased fluid in the extracellular matrix

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2
Q

hyperemia

A

increased flow

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3
Q

congestion

A

increased backup

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4
Q

hemorrhage

A

extravasation

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5
Q

hemostasis

A

keeping blood as a fluid

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6
Q

thrombosis

A

clotting blood

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7
Q

embolism

A

downstream travel of a clot

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8
Q

infarction

A

death of tissues w/o blood

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9
Q

shock

A

circulatory failure/collapse

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10
Q

fluid collection in lung

A

hydrothorax

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11
Q

fluid collection in heart

A

hydropericardium

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12
Q

fluid collection in abdominal cavity

A

ascitis

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13
Q

fluid collection in entire body

A

anascara

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14
Q

mechanism of edema

A
  1. increased vascular hydrostatic pressure
  2. decreased plasma oncotic pressure
  3. lymphatic obstruction
  4. sodium and water retention
  5. inflammation
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15
Q

increased hydrostatic pressure due to

A

impaired venous return

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16
Q

impaired venous return due to

A
  1. congestive heart failure/constrictive pericarditis
  2. cirrhosis of liver
  3. venous obstruction or compression by thrombosis, external pressure or LE inactivity
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17
Q

mechanism of congestive heart failure

A

heart not pumping blood effectively causing backing of blood in veins

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18
Q

mechanism of cirrhosis of liver

A

scarring of liver impairs return of blood through portal vein, increased back pressure in smaller veins causes ascites

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19
Q

mechanism of venous obstruction

A

back up of blood causes edema of surround tissues

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20
Q

arteriolar dilation caused by

A
  • heat

- neurohumoral dysregulation

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21
Q

reduced plasma oncotic pressure leads to

A

protein losing glomerulopathies - leaky capillaries cause loss of albumin

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22
Q

causes of reduced plasma oncotic pressure

A
  • liver cirrhosis - reduced albumin synthesis
  • malnutrition
  • protein losing gastroenteropathy
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23
Q

lymphatic obstruction leads to

A

impaired lymphatic drainage - lymphedema

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24
Q

causes of lymphatic obstruction

A
  • inflammatory
  • neoplastic
  • postsurgical
  • postirradiation
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25
Q

examples of lymphedema

A
  • filiariasis causing elephantiasis

- irradiation of breast and axilla for treatment of breast cancer causing upper limb edema

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26
Q

sodium and water retention

A

excessive water intake with renal insufficiency

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27
Q

increased tubular reabsorption of sodium (salt) occurs in

A

-renal hypoperfusion

increased oncotic pressure

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28
Q

increased salt retention causes water retention and leads to

A
  • increased hydrostatic pressure (due to intravascular fluid volume expansion)
  • decreased vascular colloid osmotic pressure (due to dilution)
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29
Q

subcutaneous edema caused by

A

cardiac or renal disease

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30
Q

pulmonary edema

A

impedes oxygen diffusion

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31
Q

brain edam caused by

A

herniation of brain stem or impedes vascular supply to brain stem

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32
Q

transudate

A

Protein and cell poor fluid
Specific gravity: less than 1.012
Protein content: less than 3 gms/dl
Lactic dehydrogenase low

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33
Q

example of transudate

A

cardiac failure and decreased protein levels

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34
Q

exudate

A

Protein and cell rich fluid
Specific gravity: more than 1.012
Lactic dehydrogenase high

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35
Q

example of exudate

A

inflammation

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36
Q

where does dependent edema occur

A

in extremities and gravity prone areas of body

ex. heart failure

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37
Q

pitting edema

A

When skin and underlying soft tissues with edema are compressed with fingers, the impressions remain

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38
Q

pitting edema is associated with

A

heart failure and is transudate

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39
Q

hypermeia and congestion caused by

A

locally increased blood volumes

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40
Q

hyperemia

A
  • active process of arteriolar dilation

- increased blood flow leading to erythema

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41
Q

example of hyperemia

A

inflammation, muscle during exercise

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42
Q

types of congestion

A
  1. passive process

2. cyanosis

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43
Q

passive process of congestion

A

reduced outflow of blood from a tissue

44
Q

cyanosis of congestion due to

A

red cell stasis and accumulation of deoxygenated Hb

45
Q

chronic passive congestion caused by — heart failure

46
Q

left heart failure causes back up of blood in

A

lungs –> lack of blood flow –> chronic hypoxia –> schema tissue injury and scarring

47
Q

what are heart failure cells

A

hemosiderin-laden macrophages found in alveoli

48
Q

acute hepatic congestion

A
  • distended central vein and sinusoids
  • ischemic centrilobular hepatocytes
  • fatty change in periportal hepatocytes
49
Q

chronic passive congestion caused by – sided heart failure

50
Q

right sided heart failure causes blood to backup in

A

liver bc R ventricle is unable to pump blood out efficiently

51
Q

gross appearance of chronic passive congestion of liver

A

centrilobular regions red-brown and slightly depressed; accentuated against zones of uncongested tan liver (nutmeg liver)

52
Q

microscopic appearance of chronic passive congestion of liver

A

sinusoidal dilation, centrilobular hemorrhagic necrosis

53
Q

hemorrhage

A

extravasation of blood into the extravascular space

54
Q

hematoma

A

hemorrhage contained within a tissue

55
Q

petechiae

A

minute 1-2 mm hemorrhages into skin, mucous membranes or serosal surfaces

56
Q

petechiae are associated with

A

locally increased intravascular pressure, low platelet counts of defective platelet function

57
Q

purpura

A

hemorrhages > 3 mm

58
Q

pupura can be associated with

A

same disorder that cause petechia

-can be secondary to trauma, vasculitis or increased vascular fragility (eg. amyloidosis)

59
Q

ecchymoses

A

larger (>1 -2cm) subcutaneous hematomas due to trauma

60
Q

ecchymoses color change caused by

A

macrophages phagocytize RBCs; hemoglobin (red-blue color) –>converted into bilirubin (blue-green color) –> hemosiderin (gold-brown color)

61
Q

clinical significane of hemorrhage depends on

A
  1. volume and rate of bleeding

2. site of hemorrhage

62
Q

large volume and rate of bleeding can cause

A

hemorrhagic (hypovolemic) shock

63
Q

intracranial hemorrhage causes increase in

A

pressure compromising blood supply or cause herniation of brainstem

64
Q

chronic or recurrent external blood loss can cause

A

anemia

eg. peptic ulcer, menstrual bleeding

65
Q

hemothorax

A

hemorrhage in pleural cavity

66
Q

hemopericardium

A

within pericardial sac

67
Q

hemoperitoneum

A

within peritoneal cavity

68
Q

shock is characterized by

A

systemic hypotension due to reduced cardiac output or reduced effective circulating blood volume

69
Q

consequence of shock

A

impaired tissue perfusion and cellular hypoxia

70
Q

cardiogenic shock due to

A

failed pumping of blood by heart

71
Q

hypovolemic shock

A

loss of blood or plasma volume (massive hemorrhage, fluid loss from severe burns) leads to low volume of blood for circulation

72
Q

septic shock results from

A

vasodilation and peripheral pooling of blood in bacterial or fungal infections

73
Q

septic shock is associated with

A

severe hemodynamic and hemostatic derangements

74
Q

at risk patients for septic shock

A

diabets

immunocompromised

75
Q

septic shock most frequently triggered by gram – bacteria

76
Q

mechanism of septic shock

A
  • free lipopolysaccharide released by degraded bacteria binds to LPS binding protein and CD14 on monocytes and macrophages
  • causes increased levels of IL-1, IL-6, TNF, IL-8
77
Q

septic shock can lead to

A
  • systemic vasodilation
  • decreased myocardial contractility
  • endothelial injury
  • activation of coagulation system
78
Q

metabolic abnormality of septic shock

A
  • insulin resistance and hyperglycemia
  • pro-inflammatory cytokines suppress insulin release while simultaneously promoting insulin resistance
  • hyperglycemia decreases neutrophil function- suppressing bactericidal activity
79
Q

in septic shock initially there is an acute surge in

A

glucocorticoid production, then there is adrenal insufficiency and a function deficit of glucocorticoids from depression of adrenal glands or frank adrenal necrosis due to DIC

80
Q

organ dysfunction of septic shock caused by

A
  • Systemic hypotension, interstitial edema, and small vessel thrombosis
  • High levels of cytokines and secondary mediators can decrease myocardial contractility and cardiac output
81
Q

increased vascular permeability and endothelial injury can lead to

A

adult respiratory distress syndrome

82
Q

severity and outcome of septic shock depends on

A

extent and virulence of infection, immune status of host, presence of other co-morbid conditions and pattern and level of mediator production

83
Q

treatment of septic shock

A
  • antibiotics
  • intensive insulin therapy for hyperglycemia
  • fluid resuscitation to maintain systemic pressures
  • corticosteroids to correct relative adrenal insufficiency
84
Q

clinical presentations of septic shock

A

Increased respiratory rate, increased heart rate, low blood pressure, fever, chills oliguria, warm skin, confusion

85
Q

toxic shock syndrome caused by

A

toxin A

-superantigen causes septic shock by widespread nonspecific activation of T cells

86
Q

clinical presentations of septic shock

A

Increased respiratory rate, increased heart rate, low blood pressure, fever, chills oliguria, warm skin, confusion

87
Q

neurohumoral mechanisms maintain cardiac output and BP by

A
  • baroreceptor reflexes
  • catecholamine release
  • renin-angiotensin axis
  • antidiuretic hormone release
  • sympathetic stimulation – body trying to maintain proper tone of vessel
88
Q

if shock continues and underlying causes are not corrected, shock progressive into

A

progressive phase

89
Q

neurohumoral mechanisms maintain cardiac output and BP by

A
  • baroreceptor reflexes
  • catecholamine release
  • renin-angiotensin axis
  • antidiuretic hormone release
  • sympathetic stimulation – body trying to maintain proper tone of vessel
90
Q

if shock continues and underlying causes are not corrected, shock progressive into

A

progressive phase

91
Q

irreversible stages of shock causes

A
  • lysosomal enzyme leakage
  • worsening myocardial contractile function
  • ishcemic bowel which may allow intestinal flora to enter circulation = may lead to bacteremic shock
  • acute tubular necrosis of kidney
92
Q

effects of lactic acidosis

A

lowers tissue pH and blunts vasomotor response

-arterioles dilate and blood beings to pool in the microcirculation

93
Q

irreversible stages of shock causes

A
  • lysosomal enzyme leakage
  • worsening myocardial contractile function
  • ishcemic bowel which may allow intestinal flora to enter circulation = may lead to bacteremic shock
  • acute tubular necrosis of kidney
94
Q

shock affects GI by causing

A
  • acute gastric petechial haemorrhages
  • ulcers
  • intestinal ischemia in border zones
95
Q

shock affects DIC

A
  • fibrin-rich microthrombi in various organs

- consumption of platelets and coagulative factors

96
Q

shock affects GI by causing

A
  • acute gastric petechial haemorrhages
  • ulcers
  • intestinal ischemia in border zones
97
Q

shock affects brain causing

A

global hypoxia ischemic encephalopahy (red neurons - dead neurons with red cytoplasm nd pyknotic nuclei)

98
Q

shock affects heart causing

A

contraction band necrosis

99
Q

shock affects kideny by

A

acute tubular necrosis

100
Q

shock affects liver by

A

centrilobular necrosis

101
Q

shock affects kideny by

A

acute tubular necrosis

102
Q

neurogenic shock caused by

A

anesthetic accident of spinal cord injury

103
Q

neurogenic shock causes

A

causes loss of vascular tone and peripheral pooling of blood

104
Q

anaphylactic shock caused by

A

IgE-mediated hypersensitivity reaction

105
Q

anaphylactic shock causes

A

widespread vasodilation, tissue hypoperfusion and hypoxia

Pathology (18 decks)

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