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Pathology Basic abcdefg > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

Circulatory disorders:

A 
Edema 
Hyperemia and Congestion
Hemorrhage
Thrombosis
Embolism
Infarction
Shock
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2
Q

% of water from body weight

A

45-75% of body weight

Young, healthy men = 50-60%
Young, healthy women = 45-50%
* decreases with age

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3
Q

Decreased Osmotic pressure
Or
Reduced plasma osmotic pressure
Causes

A 
Hypoproteinemia: liver disease
1- Protein losing glomerulopathies (nephrotic syndrome)
		2- Liver cirrhosis
		3- Malnutrition
		4- Protein losing gastroenteropathy
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4
Q

~ 5% of total body fluid is in the…

A

vascular compartment

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5
Q

The balance between vascular hydrostatic pressure and plasma colloid osmotic pressure is the driving force that maintains movement of fluids between vascular and interstitial spaces

A

Normal fluid balance

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6
Q

may occur due to clotting disorders, or from trauma

A

Bleeding

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7
Q

Normally, the exit of fluid into the interstitium at the arteriolar end is almost balanced by

A

inflow of fluid from the interstitium back into the vascular bed at the venular end

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8
Q

In normal case

The blood net flow in arteriole is

A

Out

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9
Q

A small amount of fluid stays in the interstitium because

A

of little higher hydrostatic pressure to push fluids out

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10
Q

In acute inflammation the net flow changes are

A

Net flow out in arterioles and venules and capillaries

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11
Q

increased fluid in the interstitial tissue spaces

A

Edema

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12
Q

Distribution of Body Water

In intracellular and extracellular compartments

A 
Intracellular compartment:
2/3 of body water (40% body weight) 
Extracellular compartment:
1/3 of body water (20% body weight) 
Plasma (water = 4% - 5% body weight)
Interstitial fluid (water = 15% body weight)
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13
Q

pleural effusion

A

hydrothorax

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14
Q

Venous obstruction or compression

Causes of it

A

a- Thrombosis
b- External pressure (tumor)
c- Inactivity of lower limb

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15
Q

pericardial effusion

A

hydropericardium

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16
Q

A small amount of fluid stays in the interstitium because of little higher hydrostatic pressure to push fluids out
This little amount of fluid is drained back by…

A

Lymphatics

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17
Q

ascites

A

hydroperitoneum

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18
Q

Lymphatic obstruction

Causes

A

Elephantiasis

1-Inflammatory
2- Neoplastic
3- Post-surgical
4- Post-irradiation

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19
Q

Leaky vessels

A

Inflammation

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20
Q

Impaired venous return

Causes of it

A

1- Congestive heart failure
2- Constrictive pericarditis
3- Ascites (liver cirrhosis)
4- Venous obstruction or compression

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21
Q

Arteriolar dilation

Causes of it

A

1- Heat
2- Neurohumoral disturbance
3- Inflammation

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22
Q

Edema of the dependent parts of the body (e.g., the legs when standing) is a prominent feature of

A

cardiac failure, particularly of the right ventricle

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23
Q

Myocardial cells die after

A

20-30 minutes

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24
Q

is severe and generalized edema with profound subcutaneous tissue swelling

A

Anasarca

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25
Q

In…………,diminished outflow leads to a capillary bed swollen with deoxygenated venous blood and resulting in cyanosis

A

Congestion

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26
Q

In capillaries normal case the blood net flow is

A

No net flow

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27
Q

It can be diffuse, or it may be more prominent in the regions with the highest hydrostatic pressures (the edema distribution is influenced by gravity and is termed dependent).

Finger pressure over significantly edematous subcutaneous tissue displaces the interstitial fluid and leaves a finger-shaped depression

A

I-Subcutaneous edema (pitting edema)

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28
Q

Inflammation

A

1- Acute inflammation
2- Chronic inflammation
3- Angiogenesis

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29
Q

II- Edema due to renal dysfunction or nephrotic syndrome

It may be initially manifest in tissues with a loose connective tissue matrix, e.g. eyelids, causing….

A

periorbital edema

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30
Q

The surface of the brain with ………..demonstrates widened gyri with a flattened surface. The sulci are narrowed

A

Cerebral edema

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31
Q

Inflammatory edema has a high protein content and is associated with an inflammatory reaction.

A

Exudate

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32
Q

Noninflammatory edema has a low protein content is caused by alterations in hemodynamic forces across the capillary wall (hemodynamic edema).

A

Transudate

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33
Q

Sodium Retention

Causes

A

1- Excessive Na intake with renal insufficiency
2- Increased tubular absorption of Na
a- Renal hypoperfusion
b- Increased renin-angiotensin-
aldosterone secretion

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34
Q

……….is an active process that results from increased blood flow because of arteriolar dilation.
Tissues that have………….means that they have more oxygenated blood and will appear more red

A

Hyperemia

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35
Q

It’s a passive process, it may result from impaired venous return from the tissue involved
Tissues will have deoxygenated blood
The tissue has a blue-red color (cyanosis)
Causes may be local or systemic: cardiac or hepatic

A

Congestion

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36
Q

In …….., increased inflow leads to engorgement with oxygenated blood, resulting in erythema.

A

Hyperemia

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37
Q

In both cases there is an increased volume and pressure of blood in a given tissue with associated capillary dilation and a potential for fluid extravasation

A

Hyperemia and congestion

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38
Q

In chronic passive congestion, there will be:

A

1- Stasis of poorly oxygenated blood
2- Chronic hypoxia due to impaired circulation
3- Degeneration & Death of the parenchymal cells in that tissue
4- Persistent congestion of the capillaries will cause their rupture, resulting in foci of hemorrhage
5- Red cells fragments and necrotic tissue will be phagocytosed resulting in aggregates of hemosiderin macrophages

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39
Q

In normal case

The blood net flow in venules is..

A

In

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40
Q

Increased capillary hydrostatic pressure

Causes

A

Venous obstructions
Cardiac failure

Arteriolar dilation

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41
Q

Red cells fragments and necrotic tissue will be phagocytosed resulting in ….

A

aggregates of hemosiderin macrophages

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42
Q

Hemorrhage simply means

A

bleeding

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43
Q

Capillary bleeding can occur because of

A

congestion, trauma, or inflammation

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44
Q

Collection of blood within a tissue is called

A

Hematoma

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45
Q

Large hematomas can be

A

Fatal

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46
Q

More severe than cardiac edema and affects all parts of the body equally.

A

Edema due to renal dysfunction or nephrotic syndrome

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47
Q

……..may be external or internal (within the tissues)

A

Bleeding

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48
Q

Significance of bleeding depends on:

A

the amount and the place where bleeding occurs.
Small amounts of bleeding in the cranial cavity may be fatal, whereas, 1.5 liters of blood in the stomach may pass unnoticed by the patient.

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49
Q

Rapid bleeding of up to 20% of total body blood may be

A

compensated for by the body and does not cause serious clinical manifestations

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50
Q

Slow bleeding may result in

A

iron deficiency anemia, particularly in elderly people

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51
Q

Small hemorrhages of 1-2 mm into the skin or mucous membranes .

A

Petechiae

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52
Q

Petechiae are caused because of:

A

1- increased intravascular pressure
2- low platelet count
3- defective platelet function
4- clotting factor deficiency

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53
Q

Petechial hemorrhages of the colonic mucosa, as a consequence of …ll

A

thrombocytopenia.

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54
Q

larger hemorrhages: 3-5 mm

A

Purpuras

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55
Q

Anticoagulation mechanism (Antithrombotic counter regulation) is triggered after the formation of

A

permanent clot by polymerization of fibrin and aggregation of platelets

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56
Q

Purpuras causes

A 
Causes:
1- Increased intravascular pressure
2- Low platelet count
3- Defective platelet function
4- Clotting factor deficiency 
5. Vasculitis
6. Increased vascular fragility
7. Trauma
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57
Q

Ecchymosis:

A

are subcutaneous hematoma or bruise

They are 1-2 cm in area

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58
Q

The erythrocytes in these hemorrhages are phagocytosed and degraded.

A

In Ecchymosis

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59
Q 
After the phagocytosis of ecchymosis’ erythrocytes
Their hemoglobin (red-blue in color) will be converted to ..
A

bilirubin, which is blue green in color

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60
Q

bilirubin will be converted to

A

hemosiderin, a golden-brown colored material

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61
Q

is a kind of injury, usually caused by blunt impact, in which the capillaries are damaged, allowing blood to seep into the surrounding tissue.

A

A bruise or Ecchymosis

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62
Q

Larger accumulations of blood
1-hemothorax: blood in the ….. cavity
2- hemopericardium: blood in the pericardial cavity
3- hemoarthrosis: blood in the …..
4- hemoperitoneum: blood in the peritoneal cavity

A

Pleural

Joints

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63
Q

is an areas of ischemic necrosis that is caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.

A

Infarction

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64
Q

Infarction Examples:

A 
Myocardial infarction
Cerebral infarction
Pulmonary infarction
Bowel infarction
Extremities necrosis (gangrene)
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65
Q

What vascular lesions lead to infarction?

A

[Thrombosis , Embolism ] 90%

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66
Q

Uncommon causes of infarction

A

Vasospasm of vessels: coronaries in Prinzmetal angina
Compression from outside by tumors or edema
Twisting of the vessels as in torsion of testis or intestinal intussusception or volvulus
Entrapment of vessels as in strangulated hernia
Traumatic rupture of the blood supply

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67
Q

occurs in arterial occlusions or in solid organs (such as heart, spleen, and kidney)

A

White infarcts (anemic)

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68
Q

Neurons undergo irreversible damage if they are deprived of their blood supply for

A

only 3-4 minutes

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69
Q

Infarcts are generally wedge shaped.

The apex of the wedge is at the site of the occluded vessel, and the base points towards the periphery of the organ.

A

White infarcts

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70
Q

If the base of the infarcts is a serous surface, there will be …………on that surface

A

fibrinous exudate

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71
Q

Hemorrhagic infarcts

A

Red infarcts

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72
Q

Red infarcts occur in

A

Loose tissues like lung that permits collection of blood
Tissues with dual blood supply, lungs and intestine.
Venous occlusion (e.g. ovarian torsions)
Already congested tissues from impaired venous flow (e.g. liver congestion)
Reperfusion of tissues after arterial occlusion that has caused necrosis

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73
Q

Sequence of hemostasis

A 
Vasoconstriction 
Platelet activation
Platelet aggregation
Coagulation cascade
Stable clot formation
Clot dissolution
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74
Q

EMBOLIZATION TO SMALL DISTAL VESSELS IN LUNG MAY CAUSE ISCHEMIC NECROSIS OF TISSUE OR INFARCT

A

PULMONARY INFARCT

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75
Q

Factors that affect development of infarct

A
  1. Nature of the vascular supply:
  2. Rate of occlusion development:
  3. Susceptibility of involved tissue to hypoxia:
  4. Oxygen content of the blood:
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76
Q

have end-arterial blood supply

A

spleen, kidney, and the eye

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77
Q

Have radial and ulnar blood supply

A

Upper extremities

78
Q

pulmonary and bronchial blood supply

A

Lung

79
Q

Slowly developing occlusion may give time for

A

alternative pathway

80
Q

…..Are more likely to develop infarction as compared to normal people

A

Cyanotic patients or anemic

81
Q

the process by which the blood is maintained in a clot-free fluid state and produces a local hemostatic plug at sites of vascular injury

A

Normal hemostasis

82
Q

inappropriate activation of the hemostatic process in uninjured vasculature or formation of thrombus in the setting of relatively minimal vascular injury

A

Thrombosis

83
Q

Platelet activation

Platelet aggregation

A

Primary hemostasis

84
Q

Coagulation cascade

Stable clot formation

A

Secondary hemostasis

85
Q

initial vasoconstriction is stimulated by the release of..

A

endothelin from the endothelial cells. The endothelin is an important vasoconstrictor

86
Q

results in diffuse opacification of the lung

A

Pulmonary edema

87
Q

Activation & adherence of platelets: Platelets adhere to exposed……….. via………… and are activated.

A

extracellular matrix (ECM) via von Willebrand factor (vWF)

88
Q

Activated platelets undergo a ……….change and ……….release

A

Shape change and granule release

89
Q

released…….. and……….. lead to further platelet aggregation, to form the primary hemostatic plug.

A

ADP and thromboxane A2 (TXA2)

90
Q

Local activation of the coagulation cascade (involving ………..and ……….) results in ………polymerization, reinforcing the platelets into a definitive secondary hemostatic plug.

A

(involving tissue factor and platelet phospholipids) results in fibrin polymerization

91
Q

The tissue factor (cellular lipoprotein) has the following characteristics:

A

is a pro-coagulant factor
synthesized by endothelium
is released at the site of injury

92
Q

Tissue plasminogen activator (t-PA, a fibrinolytic product) and thrombomodulin (interfering with the coagulation cascade)

A

Counter-regulatory mechanisms activated to prevent further expansion of the clot and limit the hemostatic process to the site of injury.

93
Q

Both hemostasis and thrombosis are dependent on

A

The vascular wall (Endothelium)
Platelets
The coagulation cascade

94
Q

The endothelial cells normally posses ….. properties

A

Antiplatelet, Anticoagulation, and fibrinolytic properties

95
Q

If the endothelial cells are injured or activated,

They develop

A

pro-coagulant functions
These activators increase procoagulant activity, and decrease anticoagulant activity

results in a procoagulant phenotype that contributes to localized clot formation

96
Q

Thromboplastin

A

Tissue factor

97
Q

endothelial cells activators

A

1- Cytokines: IL-1 and TNF
2- Plasma mediators
3- Infectious agents

98
Q

Endothelial cells synthesize

A 
Endothelin 
Tissue factor
PGI2 ,NO
Adenosine diphosphatase 
Heparin like molecules 
Thrombomodulin 
T-PA
vWF
99
Q

VWF helps in?

A

Platelets bind to collagen (and ECM)

100
Q

t-PA: promotes

A

fibrinolysis of the fibrin clot

101
Q

convert thrombin from procoagulant to anticoagulant

A

Thrombomodulin

102
Q

allow antithrombin to inactivate thrombin, factor Xa, and other caogulation factors

A

Heparin like molecules

103
Q

Dysfunctional endothelium may elaborate greater amounts of …..and smaller amounts of…

A

greater amounts of procoagulant factors (e.g., adhesion molecules to bind platelets, tissue factor) and smaller amounts of anticoagulant effectors (e.g., thrombomodulin, PGI2, t-PA).

104
Q

activate the coagulation cascade, the extrinsic pathway

A

Tissue factor

105
Q

PGI2 & NO

A

vasodilators and inhibit platelet aggregation

106
Q

Adenosine diphosphatase

A

degrades ADP and inhibits platelet aggregation

107
Q

Prothrombotic properties of endothelium

A

Platelets adhere to the exposed sub-endothelial collagen. This is facilitated by vWF secreted by endothelial cells
Endothelial cells secrete tissue factor which activates the extrinsic clotting pathway
Endothelium secretes plasminogen activator inhibitors which depress fibrinolysis

108
Q

At injury site, platelets come in contact with ECM and they undergo three general reactions

A

Adhesion and shape change
2- Secretion
3- Aggregation

109
Q

Genetic deficiencies of vWF (von Willebrand disease) or its receptors result

A

in serious bleeding disorders.

110
Q

thromboxane A2 (TXA2)

A

Vasoconstrictor
Secreted by platelets for platelet aggregation
In the primamry hemostatic plug nd is reversible

111
Q

formed in the coagulation cascade.
binds to platelet surface and with ADP and TXA2 causes further platelet aggregation, followed by platelet contraction and becoming irreversible (secondary hemostatic plug)

A

Thrombin

112
Q

Loss of endothelium leads to

A

Exposure of ECM
Adherence of platelets, release of tissue factor, local depletion of PGI2 and t-PA particularly important in thrombus formation in the heart and arterial circulation

113
Q

convert fribrinogen to fibrin that adds to cementing of the platelet plug

A

Thrombin

114
Q

(a cyclooxygenase inhibitor) in patients at risk for coronary thrombosis is related to its ability to inhibit the synthesis of TXA2.

A

Aspirin

115
Q

The intrinsic pathway initiated by

A

Activation of Hageman factor

116
Q

The extrinsic pathway is initiated by

A

Tissue factor

117
Q

It’s a series of reactions in which inactive proenzymes are converted into active enzymes
This results in the formation of thrombin, that converts the soluble fibrinogen into insoluble fibrin

A

Coagulation cascade

119
Q

HMWK: high-molecular-weight kininogen.

Activates

A

Hageman factor to XIIa

120
Q

Intrinsic pathway factors

A

12, 11, 9, 8

121
Q

is triggered after the formation of permanent clot by polymerization of fibrin and aggregation of platelets

A

Anticoagulation mechanism Antithrombotic counter regulation

122
Q

Extrinsic Pathway

Factors

A

Tissue factor, (7)

123
Q

Clotting is regulated in a way to be confined to the site of injury by two natural anticoagulants

A
  1. Antithrombins: (e.g., antithrombin III)

2. Protein C and S:

124
Q

It inhibits the activity of thrombin, factor IXa, Xa, XIa, & XIIa

A

Antithrombins

125
Q

Antithrombin is activated by

A

binding to heparin like molecules on endothelial cells

126
Q

They are two vitamin K dependent proteins

They inactivate cofactors Va and VIIIa

A

Protein C and S

127
Q

fibrinolytic cascade

limits the size of the final clot by activation of

A

Plasmin

128
Q

Plasmin is obtained from the precursor plasminogen either by …. or by….

A

XIIa or by plasminogen activators (mainly t-PA)

129
Q

Plasmin breaks down fibrin producing

A

fibrin split products (also called fibrin degradation products)

130
Q

Fibrinolysis is blocked by

A

Plasminogen activator inhibitors

131
Q

Causes of Thrombosis

A

Endothelial injury
Blood hypercoagulability
Stasis or turbulence of blood flow

132
Q

Common pathway factors

A

10

5,2

133
Q

Causes of endothelial cell injury:

A 
§ Physical disruption
§ Hypertension
§ Turbulent f low over scarred valves
§ Bacterial endotoxins
§ Radiation
§ Hypercholesterolemia
§ Toxic substances (e.g., cigarette smoke)
134
Q

Flow of platelets in the blood is

A

Laminar

135
Q

Turbulence or stasis will result in:

A

1) Bring platelets into contact with the endothelium
2) Prevent dilution of activated clotting factors by fresh- flowing blood
3) Promote endothelial cell activation, predisposing to local thrombosis and leukocyte adhesion
4) Delay the inflow of clotting factor inhibitors and permit the build-up of thrombi

136
Q

Hypercoagulability Conditions associated with an increased risk of thrombosis
Primary (Genetic) causes

A

1- Factor V mutations
2- Prothrombin mutations
3- Antithrombin III deficiency 4- Protein C and S deficiency

137
Q

Hypercoagulability

Secondary (Acquired) causes:

A
  1. Prolonged bed rest or immobilization
  2. Myocardial infarction , (MI)
  3. Tissue damage (surgery, fracture, burns)
  4. Cancer
  5. Prosthetic cardiac valves
  6. Disseminated intravascular coagulation (DIC)
  7. Lupus anticoagulant
138
Q

They cause obstruction of arteries and veins. They are possible sources of emboli

A

Thrombi

139
Q

…….may develop anywhere in the cardiovascular system
……. are of variable size and shape
An area of attachment to the underlying vessel or heart wall, frequently firmest at the point of origin, is characteristic of all …….

A

Thrombi

140
Q

are those thrombi that form on the walls of the heart chambers and aorta

A

Mural thrombi

141
Q

Causes of Mural thrombi

A

arrhythmias, dilated cardiomyopathy, MI, myocarditis, catheter trauma

142
Q

Lines of Zahn

A 
produced due to alternating
pale layers of platelets and
fibrin with dark layers of
RBC in thrombi formed in
the heart or aorta
143
Q

Thrombi in coronary arteries are almost always due to

A

endothelial damage resulting from atherosclerosis.

144
Q

Venous thrombosis (Phlebothrombosis)

Characteristically occur in

A

Sites of stasis

145
Q

…..May not be well attached and are prone to emboli

They contain more RBCs, therefore known as red, or stasis, thrombi

A

Venous thrombosis (Phlebothrombosis)

146
Q

Venous thrombosis (Phlebothrombosis)

90% of cases involve the veins of

A

Lower extremities

147
Q

Superficial venous thrombi usually occur in the….. particularly in….

A

the saphenous system, particularly in varicosities

148
Q

Superficial thrombi may cause swelling and pain but seldom…

A

Embolize

149
Q

……..thrombi in the large veins particularly those above the knee joint in the popliteal, femoral, & iliac veins are more serious as they may embolize

A

Deep

150
Q

……. thromboses are asymptomatic in 50% of cases. Advanced age, bed rest, and immobilization increase the risk of …….thrombosis

A

Deep vein

151
Q

Fate of Thrombus

A
  1. Propagation: thrombi may accumulate more fibrin & platelets causing obstruction
  2. Embolization: thrombi may detached and be transported to other sites in the vasculature
  3. Dissolution: thrombi may be removed by fibrinolytic activity
  4. Organization and Recanalization: Thrombi may induce inflammation and fibrosis (organization) and may become recanalized (re-establish vascular flow), or they may be incorporated into a thickened vascular wall. (in old thrombi)
152
Q

Abnormal solid mass carried in blood.

A

Embolus

153
Q 
Embolism types with example
Thromboembolism - .....
Fat - .....
Gas – ....
Liquid – ......l
A

Thromboembolism - atherosclerosis
Fat - Fractures
Gas – ‘Caisson disease’
Liquid – Amniotic fluid

154
Q

Outcome of Embolism

A

– Collateral circulation
– Infarction
– Hemorrhage

155
Q

When embolus lodges within a vessel and blocks blood supply its called

A

Embolism

156
Q

99% of all emboli represent part of thrombus, hence the commonly used term

A

Thromboembolism

157
Q

Rare forms of emboli include:

A

Droplets of fat, bubbles of air or nitrogen,
atherosclerotic (cholesterol emboli), tumor fragments,
bits of bone marrow, or foreign bodies such as bullets.

158
Q

Thromboembolism common in hospitalized patients

A

Pulmonary thromboembolism

159
Q

Pulmonary thromboembolism originates mainly in

A

Deep veins of lower extremities

160
Q

Emboli travel to the right side of the heart to the pulmonary arteries.

A

Pulmonary thromboembolism

161
Q

Pulmonary thromboembolism May be so large to block the main pulmonary artery at the site of bifurcation, called…..
Or it may be small and pass into smaller branches

A

saddle embolus

162
Q

Fate of pulmonary embolism

A
  • Sudden death, right ventricular failure, or cardiovascular collapse occur when 60% or more of the pulmonary circulation is obstructed with emboli.
  • 60-80% are clinically silent because they are small, undergo dissolution or recanalization
  • Embolic obstruction of medium-sized arteries may result in pulmonary hemorrhage
  • Multiple emboli over time may cause pulmonary hypertension with right ventricular failure
163
Q

Refers to emboli traveling within the arterial circulation

A

Systemic thromboembolism

164
Q

Systemic thromboembolism
80% arise from intra-cardiac mural thrombi associated with
left ventricular wall infarcts (2/3),with dilated left atria (1/3)
The rest originates from:

A

Atherosclerosis in aorta or from aortic aneurysms
• Paradoxical embolism: rarely, emboli may travel from venous to arterial circulation via a communication between arterial & venous circulation

165
Q

Major sites for lodging of systemic emboli:

A

the lower extremities (75%) and the brain (10%)

166
Q

…..emboli cause infarction of tissues in the distribution of the obstructed vessel

A

Arterial

167
Q

mainly after fractures of long

bones or, rarely, in the setting of soft tissue trauma and burns

A

Fat embolism

168
Q

Fat embolism symptoms

A

 Fatal in about 10% of cases
 Respiratory: tachypnea, dyspnea
 Neurological: irritability, restlessness, and coma
 Thrombocytopenia with characteristic petechiae
 It generally develops 1 to 3 days after injury
 The pathogenesis involves both mechanical obstruction and toxic injury to endothelium by FFA

169
Q

Enters the circulation from marrow after rupture of bone vascular sinusoids, or from adipose tissue through rupture of tissue venules

A

Fat embolism

170
Q

may enter the circulation during surgical obstetric procedures or as a consequence of chest wall injury
Generally, > 100 mL of ….is required to produce a clinical effect
May cause focal ischemia in the brain and heart
May cause edema, hemorrhages, and focal atelectasis or emphysema, leading to respiratory distress in the lungs

A

Air/Air embolism

171
Q

Amniotic Fluid Embolism

 The underlying cause is

A

the leakage of amniotic fluid (and its contents) into the maternal circulation via a tear in the placental membranes and rupture of uterine veins.

172
Q

Amniotic fluid embolism

The presence of the followings in the pulmonary circulation will confirm the diagnosis:

A

Squamous cells from fetal skin
Lanugo hair
Mucin derived from fetal respiratory or GI tracts

173
Q

Systemic hypoperfusion due to a reduction either in cardiac output or in the effective circulating blood volume

A

Shock (cardiovascular collapse)

174
Q

Types of shock:

A 
Cardiogenic shock
 Pump failure
Hemorrhagic (hypovolemic) shock
 Decrease in blood volume 
Septic shock
 Failure of microcirculation to retain pressure leading to wide spread peripheral vasodilatation
175
Q

Failure of myocardial pump owing to intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow

A

Cardiogenic shock

176
Q

Causes of Cardiogenic shock

A
  1. myocardial infarction
  2. cardiac tamponade
  3. outflow obstruction in pulmonary embolism 4. ventricular arrhrythmia
177
Q

Signs and symptoms: Cardiogenic shock

A 
Tachycardia
• Hypotension
• Tachypnea
• Restlessness, agitation 
• Pallor & sweating
178
Q

Results from loss of blood or plasma volume

A

Hypovolemic shock

179
Q

Causes of Hypovolemic shock

A
  1. Hemorrhage

2. Fluid loss from severe vomiting, diarrhea, burns, or trauma

180
Q

Hypovolemic shock Signs and symptoms:

A

same as in cardiogenic shock

  • Tachycardia
  • Hypotension
  • Tachypnea
  • Restlessness, agitation
  • Pallor & sweating
181
Q

Results from spread of an initially localized infection (e.g., abscess, peritonitis, pneumonia) into the bloodstream.

A

Septic shock

182
Q

Occurs when an overwhelming infection leads to low blood pressure, and vital organs may not function properly

A

Septic shock

183
Q

Has 25% to 50% mortality rate

 One of the most common causes of death in intensive care units

A

Septic shock

184
Q

Causes of Septic shock

A

Caused by systemic microbial infection:
 Most commonly (~ 70%), gram-negative infections (endotoxic shock)
 Can also occur with gram-positive and fungal infections.

185
Q

Pathogenesis of Septic Shock

A

Endotoxins are bacterial wall lipopolysaccharides (LPSs)
 LPS activate mononuclear cell with production of chemical
mediators
 The collective effect of these mediators result in:
 Fever, acute-phase reaction, neutrophilia
 Vasodilation: hypotension
 Widespread endothelial cell injury
 Activation of the coagulation system
 Multiorgan system failure

186
Q

Hemodynamic shock due to loss of vascular tone and peripheral pooling of blood resulting in vasodialtion

A

Neurogenic shock

187
Q

Initiated by a generalized immunoglobulin E-mediated hypersensitivity response
Associated with systemic vasodilatation and increased vascular permeability

A

Anaphylactic shock

188
Q

Neurogenic shock:causes of it

A

spinal cord injury or trauma

189
Q

Causes a sudden increase in the capacity of the vascular bed, which cannot be filled adequately by the normal circulating blood volume. Thus, tissue hypoperfusion and cellular anoxia result.

A

Anaphylactic shock

190
Q

Stages of Shock

A

Initial nonprogressive stage

Progressive stage

Irreversible stage

191
Q

the causative factors of shock are contained and perfusion of vital organs is maintained (adequate compensatory mechanism)

A

Initial nonprogressive stage

192
Q

tissue hypoperfusion continues, resulting in tissue hypoxia, and metabolic disturbances (e.g., anaerobic glycolysis produced lactic acidosis).

Compensatory mechanism is no longer adequate

A

Progressive stage

193
Q

the patient has multiple organ failure, and death becomes inevitable

A

Irreversible stage

Pathology Basic abcdefg (10 decks)

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