Fluid and Hemodynamic Disorders Flashcards Preview

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Flashcards in Fluid and Hemodynamic Disorders Deck (78):
1

Normal distribution of water in the body

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

Normal in/output 2.5 litres/day

2

Edema

Excess fluid in interstitial spaces and/or body cavities

Results from imbalance between hydrostatic and oncotic pressures

3

Anasarca

Generalized (non-local) edema

4

Ascites

Ash-eye-teez

Edema within the peritoneal cavities

5

Exudate

Edematous fluid rich in protein, larger molecules, cells.

Typical of inflammation

6

Transudate

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

7

What may cause the accumulation of transudate?

Increased hydrostatic pressure
Decreased oncotic pressure
Lymphatic obstruction
Sodium retention

8

Hydrostatic pressure

Promotes passage of fluids from blood vessel into interstitial fluid

Arterial end of capillary

9

Oncotic pressure

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

10

Inflammatory edema

Fluid leaks through increasingly permeable vessel wall

Acute inflammation

11

Hydrostatic edema

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

Hypertension, heart failure

12

Oncotic edema

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

Liver disease, malnutrition, nephrotic syndrome

13

Obstructive edema

Rare. Can be caused by parasites or tumours

14

Hypervolemic edema

Kidney dysfunction leading to the retention of sodium and water

15

Clinical Forms of Edema

Cerebral
Pulmonary
Pitting (of lower extremities)
Periorbital
Hydrothorax
Hydroperitoneum

16

Hyperemia

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

Three forms: active, reactive, passive

17

Active hyperemia

AKA functional hyperemia

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

Blushing, exercise, acute inflammation

18

Reactive hyperemia

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

19

Passive hyperemia

AKA congestion

Caused by venous backpressure, typically due to heart failure

Often occurs in chronic form; can lead to cyanosis

20

How much blood loss can be endured without clinical consequence?

10-15% (up to 500ml).

1000-1500 ml: shock
1500+ ml: death

21

How to tell the difference between arterial and venous blood

Arterial: bright right and under pressure, often pulsing

Venous: dark red or bluish, not pulsating

22

Hemothorax

blood in thoracic cavity

23

Hemoperitoneum

blood in peritoneal cavity

24

Hemopericardium

blood in pericardial cavity

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