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Pathology > hemodynamics > Flashcards

hemodynamics Flashcards

1
Q

hemodynamics

A

movement of blood

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2
Q

what signs of inflamm could indicate a disorder of hemodynaimcs

A

edema, hyperemia, hemorrhage

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3
Q

Hemodynamic Disorders

A

• Edema – escape of fluid
• Congestion – Abnormal accumulation of blood in tissue/organs
• Infarction – ischemic necrosis
• Shock – tissue injury secondary to systemic hypotension

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4
Q

Hemostatic Disorders

A

• Hemorrhage – escape of whole blood into tissuen
• Thrombosis – undesired clotting of blood
• Embolism – detached intravascular mass

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5
Q

Distribution of Body Water

A

• Water accounts for 60% of the lean body weight
• Total body water is distributed between the intracellular and extracellular compartments
• Intracellular compartment (40%)
• Extracellular compartment- Intravascular (5%) and Interstitial (15%)

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6
Q

Forces balancing Movement of Water Between the Intravascular and Interstitial Spaces

A

• Hydrostatic Pressure- Pressure exerted by volume of blood when confined
to a blood vessel
• Osmotic (Oncotic) Pressure- Proteins in blood vessels (Albumin)

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7
Q

where is hydrostatic pressure higher

A

Aa, outweighs osmotic= fluid out

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8
Q

where is osmotic pressure higher

A

Vv (does not change remains constant), outweighs hydrostatic= fluid in

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9
Q

residual fluid left in the ISF

A

• Outflow at the arterial end is nearly balanced by inflow at the venular end
• Residual fluid left in the interstitium is drained by lymphatic vessels

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10
Q

causes of edema

A

• Increased hydrostatic pressure or decreased plasma osmotic pressure will cause interstitial fluid to increase
• If the capacity for lymphatic drainage is exceeded, fluid accumulates (edema)

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11
Q

edema

A

swelling of tissues that result from excessive accumulation of fluid

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12
Q

locality of edema

A

• May be highly localized as occurs in a small region of skin involved with an insect bite
• May be more regionalized, involving an entire limb or a specific organ, such as the lungs (e.g., pulmonary edema)
• May be generalized, involving the whole body

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13
Q

pathophyisiological categories of edema

A

inflammatory and non-inflammatory

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14
Q

terminology of fluid accumulation
within tissues?
within thorax?
within pericardium?
within peritoneum?
generalized edema?

A

• Accumulation of interstitial fluid within the tissues= Edema
• Accumulation of fluid within body cavities
• Hydrothorax – pleural effusion
• Hydropericardium – pericardial effusion
• Hydroperitoneum – ascites
• Anasarca – generalized edema

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15
Q

• Inflammatory causes of edema

A

• inflammatory edema is caused by increased vascular permeability is a protein-rich exudate (exudate)

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16
Q

Non-inflammatory causes of edema
fluid composition?

A
  • edema caused by increased hydrostatic pressure or reduced osmotic pressure is usually protein-poor fluid (transudate)
    • Heart failure
    • Renal failure
    • Hepatic failure
    • Malnutrition
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17
Q

categories of edema fluid

A

transudate and exudate

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18
Q

edema flow chart with heart failure, renal failure, and malnutrition/ decreased hepatic syn/ nephrotic syndrome

A
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19
Q

• Exudate, leads to?

A

– high specific gravity – protein rich
• Inflammatory edema

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20
Q

• Transudate edema fluid
due to?

A

– low specific gravity – protein poor
• Due to Volume/pressure overload or Reduced plasma protein

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21
Q

categories of edema fluid

A

transudate and exudate

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22
Q

Lymphangitis

A

Lymphatic spread of bacterial infection
• Painful red streaks and regional lymphadenopathy

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23
Q

• Lymphedema

A

a term used to describe an increase in fluid in the interstitial space caused by an abnormality
in the lymphatic system

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24
Q

what is in tissues in lyphadema

A

lymphatic fluid collects in tissues causing edema

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25
Q

lymphadema congenital or acquired

A

can be either

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26
Q

acquired lymphadema from?

A

• Infection such as filariasis
• Surgery, radiation therapy

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27
Q

congenital lymphadema, example

A

due to Aplasia
• Congenital malformation of lymphatic system
• Age 1 Week: Lymphoscintigraphy exhibits no migration of radiopharmaceutical agent from right foot to right inguinal nodes
• Diagnosis: congenital aplasiaof the lymphatic system of right leg

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28
Q

axillary lymph node dissection can lead to?

A

acquired lymphadema, swollen arm

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29
Q

Stewart-Treve Syndrome

A

• Angiosarcoma arising from chronic lymphedema
• Long-standing lymphedema secondary to surgical lymph node dissection and/or radiation therapy

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30
Q

renal dx can lead to what form of edema?

A

anasarca, severe generalized edema

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31
Q

What edema(s) is seen with congestive HF

A

Pitting edema of the extremities and acities possible

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32
Q

alcoholics may have what edema?

A

Ascites in Hepatic Alcoholic Cirrhosis

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33
Q

edema danger zones

A

• Lungs - Pulmonary edema
• Brain - Cerebral edema (central nervous system)

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34
Q

cerebral edemas

A

Cerebellar Tonsil Herniation
• Increased intra-cranial pressure may result in herniation through the foramen magnum
• Compression of the medulla results in depression of the centers for respiration and cardiac rhythm control

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35
Q

what inflammatory edema can we see with dentistry

A

cellulitis secondary to dental infection

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36
Q

angioedema

A

Inflammatory Edema - Angioedema – Due to Type I Hypersensitivity Reaction

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37
Q

Localized Edema vs. Generalized Edema
causes?

A

• Localized edema is usually caused by: Increased vascular permeability (injury-inflammation)
or Obstruction of venous or lymphatic outflow
• Generalized edema is generally caused by decreased plasma osmotic pressure

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38
Q

• Increased hydrostatic pressure
leads to?
due to?

A

• Increased hydrostatic pressure = impaired venous return
• due to Congestive heart failure or Venous obstruction or compression

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39
Q

• Decreased plasma osmotic pressure (hypoproteinemia) due to?

A

• Protein-losing glomerulopathies (nephrotic syndrome)
• Liver cirrhosis (ascites)
• Protein malnutrition

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40
Q

types of lymphatic obstruction

A

• Inflammatory
• Neoplastic
• Postsurgical
• Postirradiation

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41
Q

how can sodium retention cause edema

A

• Excessive salt intake with renal insufficiency
• Increased tubular reabsorption of sodium- Renal hypoperfusion and Increased renin-angiotensin-aldosterone secretion

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42
Q

how does inflamm cause edema

A

increased permiabilty

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43
Q

Hyperemia
active or passive?
where can this occur?
color of tissues? why?

A

An active process in which arteriolar dilation leads to increased blood flow
• Sites of inflammation
• Skeletal muscle during exercise
• Affected tissues turn red (erythema) because of engorgement of vessels with oxygenated blood

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44
Q

Deep Venous Thrombosis
type of issue? passive or active?
results from?
systemic or local?
tisses appearance? why?

A

congestion issue
• A passive process resulting from reduced outflow of blood from a tissue (stasis)

• May be systemic (heart failure) or local (isolated venous obstruction)

• Congested tissues take on a dusky, reddish-blue color (cyanosis) due to red cell stasis and accumulation of deoxygenated hemoglobin

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45
Q

chronic passive congestion of liver appearence

A

nutmeg liver

46
Q

Superior Vena Cava Syndrome

A

•Compression of superior vena cava by neoplasm obstructing venous return (congestive)

47
Q

Factors Favoring Thrombosis (Virchow’s Triad)

A

• Endothelial injury
• Stasis or turbulent blood flow
• Hypercoagulability of the blood

48
Q

what determines thrombi outcome

A

• Balance between antithrombotic and prothrombotic properties of endothelium determines whether thrombus formation, propagation or dissolution occurs

49
Q

NORMALLY, endothelial cells exhibit what properties regarding thrombi

A

• Normally, endothelial cells exhibit antiplatelet, anticoagulant and antifibrinolytic properties

50
Q

how can endothelial cells be activated?
activated endothelial cells exhibit what properties?

A

• Endothelial cells may be activated by trauma, infectious agents, hemodynamic forces, plasma mediators and cytokines
• After activation, endothelial cells acquire procoagulant activities

51
Q

• Mural thrombi

A

• Mural thrombi
• Occur in heart chambers or aortic lumen

52
Q

• Arterial thrombi
• Frequently?
•most common locations
• Superimposed?

A

i
• Frequently occlusive
• Coronary, cerebral, femoral arteries, most commonly
• Superimposed on ruptured, ulcerated atherosclerotic plaque

53
Q

• Venous thrombi
• Usually?
• common location?

A

• Usually occlusive – thrombus forms a long cast of the lumen
• Veins of lower extremities

54
Q

• Vegetations

A

• Vegetations – thrombi on heart valves

55
Q

Morphology of Thrombi
attached to?
propogation?
embolization?

A

• Thrombi are focally
attached to the underlying
vascular surface
• Thrombi propagate from
the point of attachment in
the direction of blood flow
• The propagating portion
of a thrombus is often
poorly attached and is
prone to fragmentation
and embolization

56
Q

• Arterial or cardiac thrombi begin where and propogate in what direction?

A

• Begin at sites of turbulence or endothelial injury
• Propagate away from the heart

57
Q

• Venous thrombi occur at and propogate in what direction?

A

• Occur at site of stasis
• Propagate toward the heart

58
Q

Lines of Zahn
present with?
appearence/histo?
signifies?
distinguishing from post-mortem clots?

A

• Thrombi often have groosly and microscopically apparent laminations called lines of Zahn
• Pale platelet and fibrin deposits alternating with darker red cell-rich layers
• Laminations signify that a thrombus has formed in flowing blood
• Their presence can therefore distinguish antemortem thrombosis from the bland, non-laminated clots that occur postmortem

59
Q
A

lines of zahn

60
Q

venous seepage may cause

A

liver clot

61
Q

Fates of a Thrombus

A

• Dissolution – fibrinolysis (plasmin)
• Propagation – accumulate additional platelets and fibrin
• Embolization – dislodge and travel to other sites in the vasculature
• Organization and recannalization

62
Q

• Organization and recannalization of thrombus

A

• Ingrowth of endothelial cells, smooth muscle cells and fibroblasts
• Capillary channels eventually form that re-establish the continuity of the original lumen to a variable degree

63
Q

clinical problems of thrombi

A

obstruct vv and aa
embolize

64
Q

venous thrombi clinical issues

A

• Congestion and edema in vascular beds distal to the obstruction
• Embolize to lungs and cause death

65
Q

arterial thrombi clinical issues

A

• Thrombotic occlusions at critical sites (stroke, myocardial infarct) or can embolize and cause downstream infarctions

66
Q

where do most venous thrmbi occur

A

superficial or deep veins of the legs

67
Q

outcomes of superficial venous thrombi

A

cause local congestion, swelling, pain and tenderness
rarely embolize

68
Q

outcomes of DVT
offset of symptoms?
often go where?
symptomiatic? when realized?

A

• Cause local pain and edema – rapidly offset by collateral channels
• More often embolize to lungs
• Half are asymptomatic, recognized in retrospect after embolization

69
Q

risk factors of venous thrombi
coagulation?
endothelium?
bedrest?
heart?
traumas?
pregnancy?
tumors?

A

• Hypercoagulable states
• Endothelial injury
• Bedrest, immobilization
• Congestive heart failure
• Trauma, surgery, burns
• Thrombotic diathesis of pregnancy
• Neoplasia

70
Q

Risk Factors for Arterial and Cardiac Thrombi
can they embolize? where could they cause infarcts?
major cause of arterial thrombi?
Predisposition to cardiac thrombi associated with?

A

• Cardiac and aortic mural thrombi may embolize
peripherally and cause infarcts of brain, kidney and spleen
• Major cause of arterial thrombi is atherosclerosis

• Predisposition to cardiac thrombi associated with: MI, Rheumatic heart disease, and Atrial fibrillation

71
Q

Disseminated Intravascular
Coagulation (DIC)
formation of?
visable?
may cause circulatory insufficiency where?
results in decreases of?
mechanisms activated?
may evolve into?
primary dx? associated with?

A

• Formation of widespread fibrin thrombi in the microcirculation
• Thrombi not grossly visible – can be seen microscopically
• May cause diffuse circulatory insufficiency, especially in brain, heart, lungs and kidneys
• Widespread microvascular thrombosis results in platelet and coagulation protein consumption (consumptive coagulopathy)
• Fibrinolytic mechanisms are activated
• The initially thrombotic disorder may evolve into a bleeding disorder
• Not a primary disease but a potential complication of any condition associated with widespread activation of thrombin: Obstetric complication and Advanced malignancy

72
Q

embolus

A

• A detached intravascular solid, liquid or gaseous
mass that is carried by the blood to a site distant
from its point of origin
• Lodge in vessels too small to permit further passage and cause partial or complete occlusion

73
Q

embolus major consequence

A

ischemic necrosis of downstream tissue (infarction)

74
Q

• Thromboembolus

A

• Thromboembolus – almost all emboli represent
some detached part of a thrombus

75
Q

Venous and Arterial Emboli vessels sizes

A

Aa move towards decreasing sizes and Vv move towards increasing sizes

76
Q

failure on one side of the circulatory system

A

leads to increased stress on the other
(aa or vv)

77
Q

venous emboli tend to?

A

tend to lodge in one vascular bed (lung)

78
Q

Arterial emboli can travel to?

A

wide variety of sites

79
Q

arterial emboli point of arrest depends on?

A

• Point of arrest depends on source and relative amount of blood flow

80
Q

major site of arterial emboli arrest

A

lower extremities and brain

81
Q

consequences of arterial emboli arrest depend on?

A

vulnerability of tissue to ischemia, caliber of occluded vessel and collateral blood supply

82
Q

sources of arterial emboli

A

mainly athersclerosis of arteries and mural thrombi, endocarditis may contribute as well

83
Q

pulmonary embolus

A

saddle embolus- will saddle to bifurcation of the pul Aa
of greater than 60% blood flow cut off pt will die

84
Q

Paradoxical Embolus

A

• An embolus that originates on the right side venous circulation and lodges in the left side systemic arterial circulation, bypassing pul circulation

85
Q

Types of Emboli
most originate from?
bone?
air?
nitrogen?
atherosclerosis?
tumors?
amniotic fluid?
foreign bodies?

A

• Thromboemboli – most emboli are thromboembolic in origin
• Fat - bone fractures
• Bone marrow - bone fractures
• Air
• Nitrogen bubbles – decompression sickness in divers caisson disease
• Atherosclerotic debris (cholesterol emboli) -
• Tumor fragments -
• Amniotic fluid – obstetric complication
• Foreign bodies – catheters,

86
Q

Bone Marrow Embolus in the Pulmonary Circulation histo

A

embolism possesses heamtopoetic SC and marrow fat globules

87
Q

Amniotic Fluid Embolism in the
Pulmonary Circulation histo

A

fetal squamous cells

88
Q

• Infarct -

A

• Infarct - an area of ischemic necrosis caused by occlusion the
vasculature

89
Q

• Most infarcts occur from?

A

• Most infarcts occur from thrombotic or embolic arterial
occlusions

90
Q

• Venous thrombosis may cause ________, but usually just _________

A

• Venous thrombosis may cause infarction, but usually just congestion

91
Q

• Atherosclerotic vascular disease causes___% of all deaths in the United States – mostly?

A

• Atherosclerotic vascular disease causes 40% of all deaths in the
United States – mostly myocardial infarction or cerebral
infarction

92
Q

• Ischemia

A

• Restriction in blood supply, usually due to factors in
the blood vessels
• Oxygen, glucose and other blood-borne materials fail to arrive

93
Q

• Infarct

A

An area of ischemic necrosis
–Complete loss of blood supply, resulting in necrosis

94
Q

• Hypoxia

A

• More general term denoting a shortage of oxygen
• Usually a result of lack of oxygen in the air being
breathed

95
Q

Acute Transmural Myocardial Infarction results in?

A

coagulative necrosis of myocardium

96
Q

cerebral infarctions lead to? whaat form of necrosis could be seen?

A

lead to stroke and liquifactive necrosis

97
Q

remote kidney infarcts healing?

A

replacement of infarct with fibrous scar

98
Q

red infarcts

A

occurs in lung/ loose tissue with dual blood supply
vv occlusion, causes blood to collect

99
Q

Factors that Influence Development of an Infarct

A

• Nature of the vascular supply
• Rate of occlusion development
• Vulnerability of individual tissue to hypoxia
• Amount of oxygen in the blood

100
Q

white infarct

A

Aa occluded in organs with single blood supply

101
Q

Nature of the vascular supply – single vs double and development of an infarct
what tissues have single what have double?

A

dual supply tissues are less susceptible to infarcts
• Lungs – dual pulmonary artery and bronchial artery blood supply
• Liver – dual hepatic artery and portal vein circulation
• Kidney and spleen circulations are end-arterial, single supply

102
Q

• Rate of occlusion development, slowly developing allow?

A

• Slowly-developing occlusions provide time to develop
alternate perfusion pathways – collateral circulation

103
Q

Vulnerability of individual tissue to hypoxia
nn?
cardiac myocytes?
fibroblasts?

A

• Neurons – 3 to 4 minutes
• Cardiac myocytes – 20 to 30 minutes
• Fibroblasts - hours

104
Q

• Amount of oxygen in the blood and development of infarcts affected by?

A

– anemia or cyanosis

105
Q

Gangrene in Peripheral Vascular Disease
most common cause gangrene?
types of gangrene?
often associated with?

A

• Insufficient blood supply is the most common cause of gangrene
• Ischemic gangrene (dry gangrene)
• Infectious gangrene (wet gangrene)
• Often associated with peripheral vascular disease secondary to diabetes and long-term smoking

106
Q

Thrombophlebitis -
Phlebothrombosis can form where?

A

• Superficial veins
• Deep leg veins – high risk
of pulmonary embolus

107
Q

Trousseau Syndrome
due to?
considered?
leads to?
seen with?

A

• Due to Migratory thrombophlebitis (vv swelling due to thrombus)
• considered a Paraneoplastic syndrome
• Leads to: Hypercoagulability seen in pts with Adenocarcinomas (Pancreas, Colon, Lung)

108
Q

Shock
leads to?
inital damage?
prolonged?

A

• Systemic hypotension due to either reduced cardiac output or to reduced effective circulating blood volume
• Leads to impaired tissue perfusion and cellular hypoxia
• Initially reversible cellular injury
• Prolonged shock leads to irreversible cellular injury

109
Q

• Cardiogenic shock
seen in?

A

– low cardiac output due to pump failure
seen in:
• Myocardial infarct
• Ventricular arrythmias
• Extrinsic compression (cardiac tamponade)
• Outflow obstruction (pulmonary embolism)

110
Q

• Hypovolemic shock

A

– low cardiac output due to loss of blood or plasma volume
seen in:
• Massive hemorrhage
• Fluid loss from severe burns

111
Q

• Septic shock

A

– vasodilation and peripheral pooling of blood as part of a systemic immune reaction to a bacterial or fungal infection

112
Q

types of shock

A

cardiogenic
septic
hypovolemic

Pathology (19 decks)

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