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General Pathology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

What is blood hemostatis?

A
  1. Vessel Walls - balance between intravascular hydrostatic pressure and plasma colloid osmotic pressure to prevent edema
  2. Liquid blood - balance to prevent hemorrhage or thrombosis

**Body tries to keep us in hemostatic state to prevent these things from happening

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2
Q

What is edema?

A

Increased fluid in interstitial space or body cavities

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3
Q

What is hydrothorax

A

Pleural effusion (edema in lung)

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4
Q

What is hydroperitoneum

A

Ascites (edema in peritoneal cavity in abdomen)

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5
Q

What is Anasarca

A

Severe, generalized edema with profound subcutaneous swelling

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6
Q

What is Dependent edema?

A

Gravity dependent (common in congestive heart failure)

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7
Q

What is Pitting edema?

A

Finger pressure displaces interstitial fluid

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8
Q

What are the two types of edema?

A

Non-inflammatory - protein poor, transudate (getting water and electrolytes out but not cells b/c permeability has not increased)

Inflammatory - protein rich, exudate (leaky b.v. cause loss of proteins)

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9
Q

Describe the pathogenesis of edema

A

-Increased hydrostatic pressure
-Reduced plasma osmotic pressure
-Lymphatic obstruction (lymphatics normally return extra fluid back to the heart. So when these stop working, the extra fluid doesn’t get back and just pools in the interstitial space)
-Sodium retention
-Inflammation

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10
Q

Describe what normally happens in a capillary bed

A

-At the arterial end, fluid gets pushed out increasing hydrostatic pressure
-Interstitial fluid pressure is increased because of fluid coming out
-Plasma osmotic pressure in the venous end drops causing fluid to be pulled back in
-Fluid in the venous end is more dense because there is more protein component per volume of fluid than you had on the arterial end b/c some of this fluid has come out
-Fluid balance is eventually restored through lymphatics

**Problems occur when hydrostatic pressure on arterial end becomes excessive, or colloid osmotic pressure increases

(see slide 7)

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11
Q

What can cause increased hydrostatic pressure

A

Impaired venous return due to:
-Congestive Heart Failure (CHF) –> decreased blood to kidney stimulates renin/angiotensin pathway which worsens the peripheral edema
-Liver disease (ascites)
-Venous obstruction/compression: thrombosis, mass (external pressure), inactivity

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12
Q

What is the function of Renin?

A

Constricts renal b.v. and retains Na+ bringing in water

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13
Q

Describe the Renin pathway

A
  1. Any decrease in blood flow causes renin release which converts Angiotensin to Angiotensin I
  2. Angiotensin I flows through renal and stimulates ACE which converts Angiotensin I to Angiotensin II
  3. Angiotensin II causes:
    -Increased Na+ reabsorption b/c of Aldosterone secretion
    -Increased Na+ brings water with it
    -Arteriolar vasoconstriction in the kidney
    -ADH secretion from pituitary causing collection duct to absorb more water
  4. All of this leads to increased water and salt retention. Effective circulating volume increases. Perfusion of the juxtaglomerular apparatus increases.
    *The goal was to get more blood back to the kidney but if your heart is defective, then it’s not going to help.
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14
Q

What part of the heart stops functioning in someone with CHF? What does this lead to?

A

-Left ventricle
-When the left ventricle stops working, blood backs up into the lungs causing shortness of breath and tiring easily (this is the initial phase of CHF called “Left Sided Heart Failure”)
-If not treated, it will effect the R side of the heart b/c of pulmonary hypertension

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15
Q

After right sided-heart failure in CHF, what is the first place in gravity fluid will hit?

A

The liver causing enlargement of the liver

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16
Q

Describe what happens with Liver Disease

A

-Liver disease prevents blood from flowing through the heart normally
-Portal vein gets increased pressure (portal hypertension) and blood flows back to other organs leading to enlargement of the organs (intestine, stomach, spleen –> symptoms of abdominal swelling (ascites))
-With liver disease we see deoxygenated blood right around the central vein (called central lobular necrosis) b/c right on the central vein you have no oxygen so the cells die at that area. This area will gradually enlarge and then reach the portal triad and ongoing –> 1. Inferior Vena Cava, 2. Hepatic Vein, 3. Central Vein, 4. Portal Triad Vein, 5. Out to Spleen, Stomach, Abdomen

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17
Q

What causes reduced plasma oncotic pressure?

A

Decreased albumin (main blood protein) in the blood (the protein component of the blood is altered)
-Inadequate synthesis - liver disease
-Increased loss of albumin - nephrotic syndrome

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18
Q

What is the net result of reduced plasma oncotic pressure?

A

Net result is stimulation of renin-angiotensin-aldosterone pathway with Na+ and fluid retention
–> If you lose protein into your urine, the plasma oncotic pressure of blood decreases and water tends to go with it. So blood volume decrease and that stimulates renin, which tries to increase water retention but there’s no protein to go with it so you retain the water but lose it into the interstitial fluid

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19
Q

What causes lymphatic obstruction?

A

Due to inflammation or neoplastic growth
-parasitic infection (filariasis)
-breast cancer

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20
Q

What is Lymphadema?

A

Edema related to deficient lymphatics

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21
Q

What causes sodium and water retention?

A

-Acute renal failure
-Post-strep glomerulonephritis (autoimmune stimulating kidney not to work)

*Normal excretion and retention of Na+ gets thrown off. So instead of excreting the appropriate amount, you start not filtering at all and so you retain more Na+ and water over time leading to edema

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22
Q

What is the significance of edema in the brain

A

Herniation, compression of brainstem vessels, can cause death

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23
Q

What is the significance of edema in the lung

A

-Edema may occur here due to LV failure
-Causes breathing difficulty, infections

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24
Q

What is the significance of edema in the larynx

A

Airway obstruction (Ludwigs’ angina)

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25
Q

What is the significance of edema in the subcutaneous

A

May indicate RV failure, kidney dysfunction

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26
Q

What is the significance of edema in the tooth

A

Can lead to pulpal necrosis

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27
Q

What is Hyperemia

A

-“Active”
-Arteriolar dilation
-Red tissue (ex. pulpitis)

Active increase of oxygenated blood coming into a space due to arterial dilation (increased influx of blood)

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28
Q

What is Congestion

A

-“Passive”
-Decreased venous return
-Hypoxia and cyanosis –> shunting or cell death

Normal amount of fluid coming in but we’re not taking it out of the capillary bed (decreased flow on venous side) and now starts to swell with deoxygenated blood

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29
Q

List the two types of Congestion

A

Acute and Chronic

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30
Q

Describe Acute Congestion

A

-Pulmonary (lungs) - blood-filled alveoli
-Hepatic (liver) - vessel distension (enlarged)

*Build-up w/in a space preventing normal flow

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31
Q

Describe Chronic Congestion

A

-Pulmonary - hemosiderin-laden macs (by-product of RBC breaking down) and fibrosis (scar tissue). Often due to LV failure
-Hepatic - “nutmeg” liver, often due to RV failure
-Splenic - caused by liver disease

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32
Q

Describe the Chronic Congestion pathogenesis

A

-Decreased venous drainage –> increased pressure –> blood slowing OR capillaries dilate, cell survival

-Blood slowing –> hypoxia and RBCs destroyed by Macrophages

-RBCs destroyed by macrophages –> hemosiderin

-Hypoxia –> cell damage and necrosis –> fibrosis

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33
Q

What is the cause, pathogenesis, and pathology of chronic passive congestion in the lung

A

Cause: LV failure

Pathogenesis: Increased vascular pressure –> pulmonary edema

Pathology: Thickened septa, hemosiderin-laden macrophages

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34
Q

What is the cause, pathogenesis, and pathology of chronic passive congestion in the Liver

A

Cause: RV failure

Pathogenesis: Backflow from interior vena cava, stasis in liver

Pathology: Nutmeg liver, centrilobular necrosis

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35
Q

What is the cause, pathogenesis, and pathology of chronic passive congestion in the Spleen

A

Cause: Liver disease or heart failure

Pathogenesis: Backflow into spleen

Pathology: Splenomegaly, deep purple or blue; firm

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36
Q

What is a Hemorrhage?

A

Extravasation of blood from vessels into extracellular space

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37
Q

What is the pathogenesis of a hemorrhage?

A

-Trauma
-Atherosclerosis
-Inflammatory or neoplastic erosion of vessel wall
-Blood disorders (uncommon)

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38
Q

List the types of Hemorrhage

A

Hematoma (general term)
-Petechiae (1-2mm)
-Purpura (3-5mm)
-Ecchymoses (1-2cm) “bruise” or contusion
-In body cavities: hemothorax, hemoperitoneum, hemopericardium

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39
Q

Describe the pathophysiology of an internal hemorrhage

A

-RBC breakdown
–> Iron saved as hemosiderin in macrophages
–> Heme porphrin ring –> biliverdin (green) –> bilirubin (yellow)
–> Globin returns to protein pool
-Additional fluid reabsorbed
-Gross: red –> purple –> green –> yellow brown –> fades
-Can be fatal in brain or pericardium

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40
Q

Describe the pathophysiology of external hemorrhage

A

(Outside the body - mouth –> anus)
-If rapid, can cause hypovolemic shock
-Chronic (peptic ulcer, menstrual bleeding) leads to iron deficiency

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41
Q

What is hemostasis?

A

-Maintenance of blood in a fluid state with rapid formation of hemostatic plug at site of vascular injury
-Tightly regulated

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42
Q

What is Thrombosis

A

Pathologic form of hemostasis occurring in a non-traumatized vessel or where there is excessive clot formation

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43
Q

Thrombosis and Hemostasis both involve what?

A

vascular wall, platelets, and coagulation cascade

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44
Q

Describe the pathogenesis of thrombosis

A

-Endothelial cell injury or dysfunction (main factor)
-Altered blood flow (stasis and turbulence)
-Hypercoagulable blood

*May act independently or in concert

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45
Q

What does endothelial injury lead to?

A

Thrombus formation
-Direct trauma
-Ulcerated atherosclerotic plaques
-Inflammatory process (vascculitis)

46
Q

T/F: Direct epithelium loss is not required, only change in balance of pro/anti-coagulant production for thrombosis formation

A

TRUE

The epithelium can look fine but is dysfunctional. Is caused by:
-Hypertension
Scarred heart valves
-Bacterial endotoxin

47
Q

What does turbulent blood flow cause?

A

-The turbulent area is static blood
-Can have increased concentration of coagulation factors that pre-dispose you to forming a clot

48
Q

Disruption of blood flow leads to irregular flow or _____ which can injure endothelial cells

A

Turbulence

49
Q

Turbulence forms countercurrents or pockets of ______

A

Stasis

50
Q

List the consequences of stasis

A

-Promotes endothelial cell activation and leukocyte adhesion
-Prevents dilution of clotting factors and inflow of anticlotting factors
-Major factor in venous thrombi formation

51
Q

List the factors that alter blood flow (“the rocks in the river”)

A
  1. Atherosclerotic plaque - narrowing of lumen with turbulence
  2. Aneurysms (dilated vessel due to weakened wall) - lead to stasis (b/c the fluid slows down and at the edges it will stop)
  3. Atrial dilation (due to mitral valve stenosis) - leads to stasis
  4. Site of previous infarct - damaged vessels
  5. Hyperviscosity syndromes (polycythemia vera, sickle cell anemia) - prmotes coagulation
52
Q

Alteration of coagulation pathways (incresases/decreases) risk of thrombosis

A

Increases

53
Q

Describe primary (genetic) hypercoagulability

A
  1. Factor V mutation (Leiden)
    -prevents Va cleavage by Protein C (anti-thrombotic)(common pathway is staying on)
    -common in recurrent deep vein thrombosis pts
  2. Prothrombin gene mutation - increased prothrombin
  3. Protein C or S deficiency
54
Q

Describe secondary (acquired) hypercoagulability - high risk

A

Immobilization, cardiac failure, prosthetic heart valves, cancer

55
Q

Describe Antemortem thrombus

A

-Clot formed before the person died
-Firm, red (RBCs) with white (fibrin/platelet) laminations called lines of Zahn
-Focally attached to vessel wall

56
Q

Describe Postmortem thrombus (2 parts)

A

-Clot formed after death
-Dark red, soft and gelatinous portion (RBCs)
-Fat and plasma “chicken fat” portion
-Not attached to vessel wall

57
Q

What is thrombus dissolution

A

Fibrinolysis and/or retraction of the clot that can occur for recently developed thrombi

58
Q

What is thrombus organization

A

Granulation tissue formation –> remodeling into scar tissue –> incorporates into the vessel wall to reestablish blood flow (recanalization)

59
Q

What is thrombus propagation

A

Growth can lead to vessel obstruction

60
Q

What is thrombus embolization

A

Dislodging of thrombus and travel to distant site where they lodge at smallest passageway

61
Q

In both ______ and ______, blood flow is re-established w/o serous compromise

A

Dissolution and Organization/Recanalization

62
Q

What is an Embolus?

A

Detached intravascular solid, liquid or gaseous mass, carried to a distant site from its point of origin

63
Q

What can cause an embolization?

A

Can occur from fat, air/nitrogen, atherosclerotic debris (cholesterol emboli)

64
Q

What can embolization lead to?

A

Ischemic necrosis (infarction) of downstream tissue

65
Q

99% of embolization are a _______

A

detached thrombus (thromboembolus)

66
Q

Describe air emboli

A

-Gas bubbles in circulation
-During childbirth, chest wall injury or “decompression sickness”

67
Q

Describe amniotic fluid emboli

A

Torn veins during parturition

68
Q

What is venous thrombi (phlebothrombosis)?

A

-Also known as red or stasis thrombi - a lot of RBCs
-Occlusive - obstructs the vessel
-Grow downstream, in the direction of blood flow, conforming to the vessel shape
-Soft and friable, parts can break off
-90% effect leg veins

69
Q

Describe venous thrombi propagation

A

-Can lead to vessel occlusion
-May affect the superficial leg veins - swelling, pain, varicose ulcers (increase risk of infection). Superficial venous thrombi rarely embolize
-Collateral circulation typically prevents infarction in the extremities

70
Q

Describe venous thrombi embolization

A

-Arise in deep leg veins - at or above knee may embolize
-Typically travel to the lungs (pulmonary embolus)
-Can be caused by stasis induced by a hypercoagulable state (surgery, trauma, burns, cardiac failure, late pregnancy and postpartum, disseminated cancers)

71
Q

Where do most pulmonary thromboembolisms start?

A

Most from venous thrombi in the deep leg veins –> right heart –> lodge in pulmonary arteries

72
Q

Small, solitary pulmonary thrombus may….

A

dissolve or recanalize

73
Q

What can small multiple/chronic pulmonary thrombi cause?

A

Pulmonary hypertension –> dyspnea, RV failure

74
Q

What can medium pulmonary thrombi cuase?

A
  • hemorrhage –> hemoptysis
  • infarction
75
Q

What can large pulmonary thrombi cause?

A

Cardiogenic shock –> cyanosis and sudden death

76
Q

Describe arterial thrombi

A

-Occlusive, gray/white, often on top of atherosclerotic plaque, retrograde growth
-Affects the coronary, cerebral, and femoral arteries

77
Q

Describe mural thrombi

A

-Adheres to the wall of the heart, form due to abnormal contraction, trauma etc.
-Adhere to aortic wall due to aneurysm or atherosclerotic plaque

78
Q

What is the most important outcome (sequella) with Arterial/Mural thrombi?

A

Occlusion of vessels at critical sites (coronary and cerebral vessels)

-May also embolize to extremities, brain, kidneys and spleen

79
Q

Describe systemic thromboemboli

A

-Occur within the arterial circulation and usually cause infarction
-Most are from intracardiac mural thrombi (2/3 from LV infarcts, 1/4 from dilated left atria (mitral valve disease))
-Most go to the legs but can travel anywhere

80
Q

What are thrombi on heart valves also known as? What are the two types?

A

“Vegetations”

Septic and Sterile

81
Q

What are Septic thrombi?

A

Thrombotic masses filled with infectious organisms (i.e. infective endocarditis)

82
Q

What are Sterile thrombi?

A

Thrombotic mass without organisms
-Non-bacterial endocarditis in hypercoagulable state
-Verrucous endocarditis in SLE (Libman-Sack’s endocarditis)

83
Q

What is an infarction?

A

An area of ischemic necrosis

84
Q

What causes infarction?

A
  1. Arterial occlusion
  2. Venous obstruction
    -Venous thrombosis usually –> obstruction and congestion –> bypass channels open so no infarction
    -Only causes infarction in single venous outflow organs (i.e. testis, ovary)
  3. Other causes: vasospasms, swelling of an atheroma 2 degree to hemorrhage, vessel compression by tumor
85
Q

What are the types of infarcts based on?

A

Color (amount of hemorrhage) and Presence/Absence of infarction

86
Q

Describe the types of infarcts based on color

A
  1. Red (hemorrhagic) infarcts occur
    -with venous occlusion
    -in loose tissues (lung) where blood can pool
    -in tissues with dual circulation (lung, small intestine)
  2. White (anemic) infarcts occur
    -with arterial occlusion
    -in solid organs (heart, spleen and kidney)
87
Q

Describe infarcts based on presence/absence of infection

A
  1. Septic - bacterial vegetations embolize and cause an infarct that turns into an abscess
  2. Bland - without organisms
88
Q

Describe the gross infarct characteristics

A

Wedge-shaped, occluded vessel at the apex

89
Q

Describe the micro infarct characteristics

A

Ischemic coagulative necrosis with inflammatory border (liquefactive necrosis in the brain)

90
Q

Describe the aging infarct characteristics

A

Hours to days to show up. Resolves with scarring

91
Q

What are the determinants of infarction severity?

A
  1. Blood supply - most important
    -Dual circulation - Lungs (pulmonary, bronchial); Liver (hepatic artery, portal vein) or collateral circulation (legs) help prevent damage
    -End organ (Kidney, Spleen) - worse outcome
  2. Rate of development
  3. Tissue sensitivity to hypoxia - neurons are fragile (3-4 min)
  4. Oxygen content of blood - anemia, cardiovascular and pulmonary disease
92
Q

Describe Shock

A

Cardiovascular collapse (reduced cardiac output or reduced circulating blood volume) resulting in:
-hypotension
-decreased perfusion and hypoxia of tissues

93
Q

List the types of shock

A
  1. Cardiogenic
  2. Hypovolemic
  3. Neurogenic
  4. Anaphylactic
  5. Septic
94
Q

What is Cardiogenic Shock?

A

Arrhythmias, compression, pulmonary embolism

95
Q

What is Hypovolemic shock?

A

Hemorrhage, fluid loss

96
Q

What is Neurogenic shock?

A

Loss of vascular tone, sudden vasodilation and decreased BP

97
Q

What is Anaphylactic shock?

A

Type I hypersensitivity

98
Q

What is Septic shock?

A

Systemic immune response to microbial infection

*Septic shock leads to multi-organ failure!!

99
Q

What is the cause of septic shock?

A

Gram + and gram-negative bacteria and fungi

*20-30% fatal, most common cause of mortality in ICUs

100
Q

Describe the pathogenesis of septic shock

A

Pathogen-associated molecular patterns (PAMPS) are bound to cells of innate immunity (remember TLR) and are activated –> IL-1 and TNF released –> activation of endothelial cells, complement and Factor XII –>
1. thrombosis -ischemia and reduced organ perfusion
2. increased vascular permeability - edema
3. vasodilation (decreased blood pressure) - reduced organ perfusion

101
Q

List the stages of shock

A

Nonprogressive
Progressive
Irreversible

102
Q

Describe the nonprogressive stage of shock

A

Reflex mechanisms protect

103
Q

Describe the progressive stage of shock

A

Hypoperfusion –> hypoxia –> lactic acidosis. Circulatory and metabolic imbalance worsens –> DIC

104
Q

Describe the irreversible stage of shock

A

Cell survival not possible

105
Q

Organ failure with necrosis occurs in the _______

A

kidney, adrenals, liver

106
Q

Ulcers and hemorrhage occur in the ______

A

stomach

107
Q

__________ endothelial damage leaks protein out into alveoli

A

Lung - actue respiratory distress syndrome (ARDS)

108
Q

What are the physical signs/symptoms of hypovolemic, cardiogenic?

A

-Hypotension
-Weak and rapid pulse (compensating for lack of blood)
-Increased respiratory rate (b/c there’es not enough blood to carry it)
-Cool/clammy and cyanotic skin

109
Q

What is the physical signs/symptoms of septic?

A

Warm and flushed skin (b/c vasodilation systemically)

110
Q

You must discover and and control underlying causes of hemodynamic disorders to avoid _______

A

renal shutdown, GI bleed, respiratory failure

111
Q

What is the prognosis for Hypovolemic? Septic and cardiogenic?

A

Hypovolemic - 90% survival

Septic and Cardiogenic - 25% survival

General Pathology (32 decks)

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