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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
Q

Hematomas

A

blood filled swelling

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26
Q

Petechiae

A

small haemorrhages of skin and mucosa

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27
Q

Purpura

A

medium hemorrhages of skin a mucosa

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28
Q

Ecchymoses

A

large blotchy bruises

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29
Q

Hemoptysis

A

blood in respiratory tract (cough)

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30
Q

Hematemesis

A

vomiting blood

may be due to esophogeal cancer

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31
Q

Melena

A

Black, discoloured blood in stool.

May be due to stomach cancer

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32
Q

Hematochezia

A

Anorectal bleeding

May be due to hemmorrhoids

33
Q

Metrorrhagia

A

uterovaginal bleeding

cervical or uterine cancer

34
Q

Menorrhagia

A

heavy menstrual bleeding

endometriosis

35
Q

Hematuria

A

blood in urine

kidney infection

36
Q

Vomiting blood

A

Hematemesis

37
Q

Coughing blood

A

Hemoptysis

38
Q

Anorectal bleeding

A

Hematochezia

39
Q

Black discoloured blood in stool

A

Melena

40
Q

Blood in urine

A

Hematuria

41
Q

Uterovaginal bleeding

A

Metrorrhagia

42
Q

Thrombosis

A

Transformation of fluid into solid

Clotting of whole blood into blood cells and fibrin

43
Q

Fibrin

A

Polymerized fibrinogen.

Forms a network of think filaments that bind together the cellular elements of blood, forming a thrombus.

44
Q

Thrombus

A

Hemostatic plug

Only forms in living creatures.

45
Q

What promotes thrombosis?

A

Clotting factors

Platelets

46
Q

What inhibit/counteract thrombosis?

A

Endothelial cells

Plasmin.

47
Q

Intervascular coagulation is the result of interaction between:

A
  1. Coagulation proteins
  2. Endothelial cells
  3. Platelets.
48
Q

Role of coagulation proteins in thrombosis

A

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
Q

Role of endothelial cells in hemostasis

A

Normally secrete antithrombic substances.

When injured (activated by injury or trauma) become procoagulant

Activated by cytokines (IL-1 or TNF)

50
Q

Role of platelets in thrombosis

A

Neutralize heparin and other anticoagulant factors

secretes thromboxane

Stimulates coagulation.

51
Q

Heparin

A

Blood thinner

52
Q

Thromboxane

A

In platelet plug formation, a prostaglandin “liberated” by platelets

Activates nearby platelets
Cause vasoconstriction

Directly stimulates coagulation process

53
Q

Plasmin

A

Thrombolytic chemical.

Degrades small thrombi

54
Q

Virchow’s Triad

A

Predisposing conditions for pathological thrombi

  1. Endothelial cell injury
    2 Hemodynamics changes
  2. Hypercoagulability of whole blood
55
Q

Endothelial cell injury

A

Part of Vichow’s triad

Under influence of SMIs endothelium go from anticoagulant to thrombogenic

56
Q

Hemodynamics changes

A

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
Q

Hypercoagulability of blood

A

Part of Vichow’s triad

Often due to changes in fluid balance/hemoconcentration (burns, Cancer, cardiac failure, bun in oven).

58
Q

Thrombi classified by location

A

Intramural

Valvular (debilitated persons; sterile thrombotic endocarditis)

Arterial (contributes to atherosclerosis/aneurysms)

Venous (common in varicose veins; DVTs)

Microvascular (typical of DIC/shock)

59
Q

Red (conglutination) thrombi

A

Thrombi in small vessels are red composed of tightly intermixed RBCs and fibrin.

60
Q

Layered (sedimentation) thrombi

A

Distinct layers of cellular elements and fibrin

In large arteries, vein, mural thrombi

61
Q

Lines of Zahn

A

In layered thrombi, the white lines. Made up of fibrin and platelets.

62
Q

Fate of thrombi

A
  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
Q

Most common cause of myocardial infarction

A

Sudden thrombotic occlusion

64
Q

Clinical correlations of thombosis

A 
Myocardial infarction
Chronic heart failure
Embolus
Infarct
Stroke (cerebral infarct)
Septic emboli
65
Q

Embolus

A

freely moveable, intravascular mass that is carried from one anatomical site to another via the blood

(emboli – plural)

66
Q

Embolism

A

infarct caused by embolus

67
Q

Thromboemboli

A

thrombi carried by venous or arterial blood

*only clinically significant emboli

68
Q

Liquid emboli

A

more squishy than liquid

fat emboli following bone fracture
amniotic fluid emboli in veins

69
Q

Venous emboli

A

typically lodge in pulmonary artery and cause pulmonary embolism

smaller emboli can cause pulmonary infarcts (–> sub pleural pain)

70
Q

Arterial emboli

A

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
Q

Gaseous embolism

A

air injected into veins, or air liberated under decreased pressure (caisson disease or decompression sickness)

72
Q

Solid particle emboli

A

cholesterol, tumour cells, bone marrow

73
Q

Infarction

A

Sudden insufficiency of blood supply leading to local necrosis

Usually caused by thrombi or thromboemboli

Arterial vs venous
Red vs white

74
Q

Renal infarct

A

associated with hematuria

75
Q

Intestinal infarct

A

Can cause gangrene – medical emergency

76
Q

White infarct

A

Typical of solid organs (heart, kidneys, spleen)

Ischemic necrosis paler than surrounding tissues

77
Q

Red infarct

A

Typical of venous infarction, particularly of intestines or testes

78
Q

Fate of infarcts

A

Ischemic necrosis irreversible

Liquifactive necrotic tissue can be resorbed and leave clear fluid-filled cyst

Gen Path 300 (8 decks)

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