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Gen Path 300 > Fluid and Hemodynamic Disorders > Flashcards

Fluid and Hemodynamic Disorders Flashcards

1
Q

Normal distribution of water in the body

A

60% total body weight
2/3 intracellular
1/3 extracellular (interstitial or circulating)

Normal in/output 2.5 litres/day

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2
Q

Edema

A

Excess fluid in interstitial spaces and/or body cavities

Results from imbalance between hydrostatic and oncotic pressures

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3
Q

Anasarca

A

Generalized (non-local) edema

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4
Q

Ascites

A

Ash-eye-teez

Edema within the peritoneal cavities

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5
Q

Exudate

A

Edematous fluid rich in protein, larger molecules, cells.

Typical of inflammation

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6
Q

Transudate

A

Edematous fluid which contains less protein than exudate, and low in cells and other large molecules

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7
Q

What may cause the accumulation of transudate?

A

Increased hydrostatic pressure
Decreased oncotic pressure
Lymphatic obstruction
Sodium retention

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8
Q

Hydrostatic pressure

A

Promotes passage of fluids from blood vessel into interstitial fluid

Arterial end of capillary

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9
Q

Oncotic pressure

A

aka Colloid Oncotic Pressure

Promotes passage of fluid from interstitial fluid to blood vessel

Due to relatively high concentration of colloids (large molecules) in blood vessel

Venue end of capillary

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10
Q

Inflammatory edema

A

Fluid leaks through increasingly permeable vessel wall

Acute inflammation

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11
Q

Hydrostatic edema

A

Intravascular pressure promotes transmembranous passage of fluids. Increased venous back pressure

Hypertension, heart failure

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12
Q

Oncotic edema

A

Decreased concentration of plasma proteins (specifically albumin) in blood vessel/ decrease in colloid osmotic pressure

Liver disease, malnutrition, nephrotic syndrome

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13
Q

Obstructive edema

A

Rare. Can be caused by parasites or tumours

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14
Q

Hypervolemic edema

A

Kidney dysfunction leading to the retention of sodium and water

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15
Q

Clinical Forms of Edema

A 
Cerebral
Pulmonary
Pitting (of lower extremities)
Periorbital
Hydrothorax
Hydroperitoneum
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16
Q

Hyperemia

A

Increase of blood flow due to the presence of metabolites and/or a change in general conditions

Three forms: active, reactive, passive

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17
Q

Active hyperemia

A

AKA functional hyperemia

Increased blood flow that occurs when tissue is active and requires more metabolites

Blushing, exercise, acute inflammation

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18
Q

Reactive hyperemia

A

Occurs in response to a profound increase in blood flow to an organ after being occluded

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19
Q

Passive hyperemia

A

AKA congestion

Caused by venous backpressure, typically due to heart failure

Often occurs in chronic form; can lead to cyanosis

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20
Q

How much blood loss can be endured without clinical consequence?

A

10-15% (up to 500ml).

1000-1500 ml: shock
1500+ ml: death

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21
Q

How to tell the difference between arterial and venous blood

A

Arterial: bright right and under pressure, often pulsing

Venous: dark red or bluish, not pulsating

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22
Q

Hemothorax

A

blood in thoracic cavity

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23
Q

Hemoperitoneum

A

blood in peritoneal cavity

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24
Q

Hemopericardium

A

blood in pericardial cavity

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25
Hematomas
blood filled swelling
26
Petechiae
small haemorrhages of skin and mucosa
27
Purpura
medium hemorrhages of skin a mucosa
28
Ecchymoses
large blotchy bruises
29
Hemoptysis
blood in respiratory tract (cough)
30
Hematemesis
vomiting blood may be due to esophogeal cancer
31
Melena
Black, discoloured blood in stool. May be due to stomach cancer
32
Hematochezia
Anorectal bleeding May be due to hemmorrhoids
33
Metrorrhagia
uterovaginal bleeding cervical or uterine cancer
34
Menorrhagia
heavy menstrual bleeding endometriosis
35
Hematuria
blood in urine kidney infection
36
Vomiting blood
Hematemesis
37
Coughing blood
Hemoptysis
38
Anorectal bleeding
Hematochezia
39
Black discoloured blood in stool
Melena
40
Blood in urine
Hematuria
41
Uterovaginal bleeding
Metrorrhagia
42
Thrombosis
Transformation of fluid into solid Clotting of whole blood into blood cells and fibrin
43
Fibrin
Polymerized fibrinogen. Forms a network of think filaments that bind together the cellular elements of blood, forming a thrombus.
44
Thrombus
Hemostatic plug Only forms in living creatures.
45
What promotes thrombosis?
Clotting factors Platelets
46
What inhibit/counteract thrombosis?
Endothelial cells Plasmin.
47
Intervascular coagulation is the result of interaction between:
1. Coagulation proteins 2. Endothelial cells 3. Platelets.
48
Role of coagulation proteins in thrombosis
Involved in intrinsic and extrinsic pathways of blood clotting. Leads to creation of thrombin, which catalyzes transformation go fibrinogen into fibrin. Fibrin is framework for clot.
49
Role of endothelial cells in hemostasis
Normally secrete antithrombic substances. When injured (activated by injury or trauma) become procoagulant Activated by cytokines (IL-1 or TNF)
50
Role of platelets in thrombosis
Neutralize heparin and other anticoagulant factors secretes thromboxane Stimulates coagulation.
51
Heparin
Blood thinner
52
Thromboxane
In platelet plug formation, a prostaglandin "liberated" by platelets Activates nearby platelets Cause vasoconstriction Directly stimulates coagulation process
53
Plasmin
Thrombolytic chemical. | Degrades small thrombi
54
Virchow's Triad
Predisposing conditions for pathological thrombi 1. Endothelial cell injury 2 Hemodynamics changes 3. Hypercoagulability of whole blood
55
Endothelial cell injury
Part of Vichow's triad Under influence of SMIs endothelium go from anticoagulant to thrombogenic
56
Hemodynamics changes
Part of Vichow's triad Two kinds: 1 Disturbance of blood flow (Turbulence and margination) 2 Slowing of blood flow (Sedimentation and blood eddies)
57
Hypercoagulability of blood
Part of Vichow's triad Often due to changes in fluid balance/hemoconcentration (burns, Cancer, cardiac failure, bun in oven).
58
Thrombi classified by location
Intramural Valvular (debilitated persons; sterile thrombotic endocarditis) Arterial (contributes to atherosclerosis/aneurysms) Venous (common in varicose veins; DVTs) Microvascular (typical of DIC/shock)
59
Red (conglutination) thrombi
Thrombi in small vessels are red composed of tightly intermixed RBCs and fibrin.
60
Layered (sedimentation) thrombi
Distinct layers of cellular elements and fibrin In large arteries, vein, mural thrombi
61
Lines of Zahn
In layered thrombi, the white lines. Made up of fibrin and platelets.
62
Fate of thrombi
1. Lysis and resolution 2. Organization. Granulation replaced by collagenous fibrous tissue 3. Recanalization 4. Can break off an embolize (which can lead to infarction).
63
Most common cause of myocardial infarction
Sudden thrombotic occlusion
64
Clinical correlations of thombosis
``` Myocardial infarction Chronic heart failure Embolus Infarct Stroke (cerebral infarct) Septic emboli ```
65
Embolus
freely moveable, intravascular mass that is carried from one anatomical site to another via the blood (emboli -- plural)
66
Embolism
infarct caused by embolus
67
Thromboemboli
thrombi carried by venous or arterial blood *only clinically significant emboli
68
Liquid emboli
more squishy than liquid fat emboli following bone fracture amniotic fluid emboli in veins
69
Venous emboli
typically lodge in pulmonary artery and cause pulmonary embolism smaller emboli can cause pulmonary infarcts (--> sub pleural pain)
70
Arterial emboli
Common cause of ischemia in spleen, kidney and intestines Usually originates from cardiac mural or valvular thrombi Mechanically fragmented because of fast arterial blood flow --> tend to lodge in small and medium sized arteries (esp middle cerebral artery --> basal ganglia infarcts)
71
Gaseous embolism
air injected into veins, or air liberated under decreased pressure (caisson disease or decompression sickness)
72
Solid particle emboli
cholesterol, tumour cells, bone marrow
73
Infarction
Sudden insufficiency of blood supply leading to local necrosis Usually caused by thrombi or thromboemboli Arterial vs venous Red vs white
74
Renal infarct
associated with hematuria
75
Intestinal infarct
Can cause gangrene -- medical emergency
76
White infarct
Typical of solid organs (heart, kidneys, spleen) Ischemic necrosis paler than surrounding tissues
77
Red infarct
Typical of venous infarction, particularly of intestines or testes
78
Fate of infarcts
Ischemic necrosis irreversible Liquifactive necrotic tissue can be resorbed and leave clear fluid-filled cyst

Gen Path 300 (8 decks)

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