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Pathology block 2 > Hemodynamics I > Flashcards

Hemodynamics I Flashcards

1
Q

Define edema

A

swelling of tissue due to increased fluid in interstitial tissue spaces

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2
Q

Define ascites

A

fluid in the abdominal cavity

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3
Q

Anasarca:

A

generalized edema

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4
Q

Hyperemia:

A

(erythema) an active increase in arterial blood flow

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5
Q

Congestion:

A

passive decrease in venous outflow

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6
Q

Hemorrhage:

A

extravasation of blood due to blood vessel rupture

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7
Q

Hematoma:

A

hemorrhage enclosed within tissue

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8
Q

Petechiae:

A

tiny (1-2 mm) hemorrhages due to platelet deficiency

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9
Q

Hemostasis:

A

(1) the maintenance of blood in a free-flowing liquid state in normal blood vessels and (2) the formation of a blood clot (hemostatic plug) at a site of vascular injury

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10
Q

Platelets:

A

anucleate cellular components of blood important in initiation and propagation of clotting

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11
Q

Thrombosis:

A

inappropriate formation of blood clot in a blood vessel (usually occlusive)

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12
Q

Hypercoagulability:

A

an abnormal tendency to form blood clots

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13
Q

Coagulopathy:

A

an abnormal tendency to bleed

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14
Q

Embolism:

A

a detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin

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15
Q

Infarction:

A

an area of ischemic necrosis

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16
Q

Describe the presentation and cause of edema

A

it can be localized or generalized

common cause of generalized edema is heart failure

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17
Q

What is a hydrothorax?

A

fluid in the pleural cavity (pleural effusion)

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18
Q

Generalized edema due to, for instance, renal failure may appear initially where?

A

in tissues with a loose connective tissue matrix such as around the eyes, causing periorbital edema.

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19
Q

What is the 1st sign of nephrotic syndrome?

A

periorbital edema noticed by the mother of a 2-6 yr old which is the age range which is typically noted

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20
Q

How can you test for pitting edema?

A

If finger pressure on edematous subcutaneous tissue leaves a temporary impression

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21
Q

What are the 5 pathophysiologic categories of edema?

A

(1) increased hydrostatic pressure,
(2) decreased plasma osmotic pressure,
(3) lymphatic obstruction,
(4) sodium retention,
(5) inflammation.

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22
Q

The four most common causes of edema are

A
  1. increased hydrostatic pressure,
  2. decreased plasma oncotic pressure,
  3. sodium retention
  4. inflammation.
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23
Q

***What causes leg edema? lung? general lower body?***

A

increased hydrostatic pressure due to deep venous thrombosis

if edema is in lungs then it is due to left heart failure

if it is in the lower body then due to right heart failure

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24
Q

Describe dependent edema

A

distribution is not specific for increased hydrostatic pressure but edema is worse in the legs when standing and worse in thesacrum when recumbent

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25
Q

Describe how the heart and kidneys can cause 2 different types of edema at the same time

A
  1. Heart failure causes decreased renal blood flow,
  2. which activates the renin-angiotensin-aldosterone system.
  3. Increased aldosterone causes retention of sodium (and water),
  4. then causes edema due to sodium retention,
  5. creating edema of two different types at the same time.
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26
Q

Edema from decreased plasma osmotic pressure is a feature of what?

A

the nephrotic syndrome due to protein loss through the kidneys

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27
Q

Edema from hepatic cirrhosis is due to what?

A

increased hydrostatic pressure in the portal venous system

decreased plasma osmotic pressure due to protein loss into ascites and deficient hepatic protein synthesis.

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28
Q

What is the major protein for maintaining plasma oncotic pressure?

A

albumin which accounts for nearly half of the total plasma protein

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29
Q

How does severe hypoalbuminemia lead to more decreased plasma oncotic pressure?

A

causes secondary hyperaldosteronism (like heart failure), adding an element of edema due to sodium retention to the edema of decreased plasma oncotic pressure.

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30
Q

Describe edema due to sodium retention. What usually causes it?

A

always generalized, with increased hydrostatic pressure (and, to a lesser extent, dilutional decrease in plasma osmotic pressure).

It is usually caused by heart failure (or renal failure).

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31
Q

Describe edema due to inflammation

A

can be localized (at site of infection) or generalized (with SIRS or sepsis).

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32
Q

What is lymphedema? Describe its location in the body

A

due to lymphatic obstruction.

It is usually localized and caused by tumor, inflammation, surgery, radiation or scar.

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33
Q

What will lymphedema due to breast cancer look like?

A

can make the skin resemble an orange peel

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34
Q

What is the main and secondary causes of pulmonary edema?

A

The most common cause of pulmonary edema is left heart failure;

other causes include the acute respiratory distress syndrome (ARDS), hypersensitivity reactions, pneumonia and renal failure.

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35
Q

What does pulmonary edema look like when it is in the alveoli?

A

clear frothy fluid (pink if blood is mixed in it) in the alveoli (airspaces)

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36
Q

When does pulmonary edema become more severe?

A

when the clear frothy fluid reaches the airways

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37
Q

What is the major symptom of pulmonary edema? sign?

A

The major symptom of pulmonary edema is dyspnea (shortness of breath)

the major sign is pulmonary crackles (an inspiratory crackling sound on listening to the lungs with a stethoscope, formerly called “rales”).

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38
Q

T/F cerebral edema can be localized or generalized. describe

A

true

localized => (around an abscess or tumor) or generalized (with encephalitis, etc.)

Generalized brain swelling causes swollen gyri and narrow sulci over all of the hemispheres.

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39
Q

When can cerebral edema be fatal?

A

if it is due to herniation (protrusion) of cerebellar tonsils into foramen magnum compressing the brainstem respiratory center.

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40
Q

What is this an example of?

A

Hyperemia

(due to photosensitivity)
[note the red color]
{arterial}

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41
Q

What is this an example of?

A

Congestion

(due to superior vena cava obstruction)
[note the blue color] => {venous}

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42
Q

What is the primary cause of hyperemia and what are the results?

A

Inflammation is the overwhelmingly most common cause of hyperemia.

Hyperemia causes an abnormal reddish coloration due to the presence of excess oxygenated blood in a tissue.

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43
Q

What is the result of congestion?

A

Congestion causes cyanosis, an abnormal bluish coloration due to the presence of excess deoxygenated blood in a tissue.

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44
Q

Cyanosis can occur without congestion. Describe cyanosis due to lungs

A

Failure of the lungs to load the blood with oxygen can cause cyanosis, but this cyanosis due to pulmonary failure is generalized and referred to as “central”.

An anatomic abnormality that causes venous blood to bypass the lungs and reenter the arterial circulation without acquiring any oxygen in the lungs can also cause central cyanosis.

45
Q

How can cyanosis due to CV or pulmonary disease be noticed?

A

Cyanosis due to cardiovascular or pulmonary disease tends to be first visible around the lips.

The nailbeds are another site where central or peripheral cyanosis may be visible early.

46
Q

What causes passive congestion of the liver? when is it worst?

A

Right heart failure due to the backup of blood inadequately pumped by the heart

passive liver congestion is first and worse in the centrilobular areas

47
Q

Passive congestion of the liver is grossly identified how?

A

gross pathological finding of “nutmeg liver” consisting of alternating red and tan tissue causing the cut surface of liver to resemble the cut surface of a nutmeg

Grossly visible nutmeg liver usually shows hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas.

48
Q

Why should nutmeg liver with centrilobular chronic passive congestion not be considered?

A

hepatic lobules are microscopic.

nutmeg liver can be acute.

the necrosis causing the nutmeg appearance is mostly due to inadequate arterial perfusion of the liver.

49
Q

Chronic sublethal left heart failure causes what in the lung?

A

hemophages to accumulate in pulmonary alveoli

(with iron from blood that has leaked into the alveoli due to capillaries burst from the high pressure).

50
Q

Are hyperemia and congestion life threatening in the vessels?

A

No => Hyperemia and congestion both feature liquid blood in blood vessels

just an abnormally large amount of blood where it belongs.

51
Q

What is a hemothorax?

A

hemorrhage into a pleural cavity

52
Q

What is a hemopericardium?

A

hemorrhage into the pericardial space

53
Q

What is a hemoperitoneum?

A

hemorrhage into the abdominal cavity

54
Q

What is a hemathrosis?

A

hemorrhage into a joint

(generally associated with hemophilia)

55
Q

What is hemostasis regulated by?

A
  1. vascular wall (endothelium)
  2. platelets
  3. coagulation cascade
56
Q

What do platelets contain that are important for hemostasis?

A
  1. ADP
  2. fibrinogen
  3. clotting factors V and VIII
  4. calcium
  5. epinephrine
57
Q

List the 4 stages of hemostasis at site of vascular injury

A
  1. vasoconstriction
  2. primary hemostasis
  3. secondary hemostasis
  4. throbus and antithromboti events
58
Q

Describe the vasoconstriction stage of hemostasis

A

brief arteriolar vasoconstriction mediated by reflex neurogenic mechanisms augmented by local secretion of vasoconstrictors such as endothelin

endothelin is a potent endothelium derived vasoconstrictor

59
Q

Describe the primary hemostasis stage at the site of a vascular injury

A

plate adhesion to thrombogenic extracellular matrix takes place

platelet adhesion to ECM is mediated by von Willebrand factor which binds to their GpIb receptors

adhesion is associated with a change in shape of platelets from smooth surfaced discs to spheres with numerous long spiky projections which facilitate the platelets sticking aggregating

the change in the GpIIb/IIIa receptors allows binding to fibrinogen which binds them causing them to link and aggregate

60
Q

In primary hemostasis, platelet activation is done by platelet granule release of what? what does this cause?

A

platelet activation is associaed with release of ADP and thromboxane A2

this causes additional platelet recruitment and aggregation resulting in primary hemostatic plug

61
Q

What activates the coagulation cascade in secondary hemostasis?

A

tissue factor (membrane-bound procoagulant made by endothelium) and platelet factors

tissue factor is clotting factor III

62
Q

What does the coagulation cascade culminate in?

A

the conversion of fibrinogen to fibrin by activated thrombin

thrombin stimulates platelets to release thromboxane A2, activates monocytes, and lymphocytes

it also stimulates endothelial cells to adhere to neutrophils and to release NO, tissue plasminogen activator and prostacyclin

63
Q

Describe stage 4 wrt thrombus stabilization and antithrombotic events

A

solid permanent plug of aggregated platelets and polymerized fibrin is formed

64
Q

What are the counter regulatory mechanisms that limit the hemostatic plug to the site of injury?

A

the expression of thrombomodulin on the surface of endothelial cells

thrombomodulin binds thromin & thus activating protein C

fibrinolytic system breaks does thrombi which includes tissue plasminogen activator, plasmin tissue factor pathway inhibitor, antithrombin III, heparin-like molecules, protein S, urokinase

65
Q

Deficiency of von Willebrnad factor is a disease associated with deficiencies of many of these anti-coagulant and pro-coagulant factors. Describe it.

A

leads to tendency to bleed with surgery or menstration

66
Q

What does overactivity of von Willebrand factor due to?

A

overactivity is due to abnormally large multimers of it leads to a tendency to clot in small blood vessels and then bleed from having used up too many platelets and clotting factors

67
Q

If you have deficiency of GpIb receptors for von Willebrand factor, what occurs? deficiency of platelet GpIIb/IIIa receptors?

A

GpIb => cuases bleeding tendency

GpIIb/IIIa cuase bleeding tendency due to deficient platelet aggregation

68
Q

Snake venoms mimick what disease of bleeding?

A

platelet GpIIb/IIIa receptors

69
Q

What does ADP do wrt coagulation?

A

induces the conformational change that mediates the binding of platelet GpIIb/IIIa receptors to fibrinogen and in aggregation

70
Q

How does Clopidogrel work? and how is it taken?

A

blocks platelt ADP receptors and is taken orally by patients who have suffered clotting of their critical coronary or cerebral arteries

71
Q

What are the 3 predisposing factors to thrombosis? which is the most important?

A
  1. endothelial injury (most important)
  2. abnormal blood flow
  3. hypercoagulability
72
Q

What effect does smoking have on coagulation?

A

hemodynamic stress of hypertension or toxicity of hypercholesterolemia or produces absorbed from smoking can increase endothelial procoagulant factors or decrease their anticoagulant foactors enough to cause thrombosis

73
Q

What types of abnormal blood flow occur in thrombosis? How do each act?

A

Turbulent blood flow over ulcerated atherosclerotic plaques promotes arterial thrombosis

Stasis promotes areterial thrombosis in arterial aneurysms

74
Q

WRT sickle cell disease, polymerization of the abnormal hemoglobin deforms the RBCs, what is the result?

A

they get stuck in small blood vessels and this occlusion leads to stasis predisposing to thrombosis

75
Q

Where does thrombosis commonly occur? Where is it most serious?

A

more common in veins

more serious in arteries

76
Q

Hypercoagulable states predispose to venous thrombosis. How is Factor V Leiden mutation related?

A

it is the most common inherited hypercoagulable state (5% whites)

Heterozygotes hav e 5x higher risk of venous thrombosis

homozygotes have a 50x increased risk

mutation in clotting factor V akes it resistant to activated protein C which will result in the loss of an important clot-limiting counter-regulatory mechanism

77
Q

How is prothrombin G20210A mutation associated with hypercoagulable states?

A

2nd most common inherited hypercoagulable state and confers to 3x increase risk of venous thrombosis

78
Q

What are the common acquired hypercoaguable states?

A

surgery, cancer, antiphospholipid Ab syndrome

79
Q

In what ways does cancer contribute to the hypercoagulable state in a patient?

A

partily due to inflammatory response to malignant tumors but often these tumors outgrow their blood supply and have some necrosis

this will lead to release of highly thombogenic necrotic debris into general ciruculation

malignant tumors will compress veins or invade them, partially or completely obstructing blood flow in them, creating turbulent flow or stasis

80
Q

What are the 6 hypercoagulable states which are congenital?

A
  1. Factor V Leiden mutation
  2. Prothrombin gene mutation
  3. Methyl-tetra-hydro-folate reductase gene mutation
  4. Anti-thrombin 3 deficiency
  5. Protein C deficiency
  6. Protein S deficiency
81
Q

Which hypercoagulable states are acquired?

A
  1. surgery
  2. cancer
  3. trauma
  4. bed ridden state
  5. disseminated intravascular coagulation
  6. heparin-induced thrombocytopenia
  7. anti-phospholipid syndrome
82
Q

Antiphospholipid Ab syndrome is a rare disease and life-threatening in the acquired hypercoagulable state. Describe the most common prevalence and a few reasons why this occurs

A

It causes arterial thrombosis and generally in young females with autoimmune disease

patients have Abs against phospholipids associated with SLE

When patients have this disease, around 5% in pregnant women with a range of up to 15% having recurrent miscarriages

83
Q

Surgery to treat morbidity causes what? 2 specifics

A

causes morbidity via hypercoagulability and adhesions

84
Q

What are the 3 types of thrombi (blood clots)? describe them

A
  • arterial thrombi tend are rich in platelets (“white thrombi”)
  • venous thrombi are rich in erythrocytes (“red thrombi”)
  • “Mural thrombi” are located on the wall of the heart
85
Q

Where do arterial thrombi occur usually?

A

sites of endothelial injury

86
Q

Describe the common location and growth tendencies of venous thrombi. What exam can diagnose these?

A

commonly occur at sites of stasis

grow on hte side closer to the heart

most likely to break off and be carried with the bloodstream

ultrasound exams are the standard modality for diagnosing deep vein thrombosis in legs but obesity frequently causes false negatives

87
Q

What are “vegetations”? What category are they in?

A

thrombi on the heart valves

mostly in category of non-bacterial thrombotic endocarditis until they are infected then move into the category of infective endocarditis

some however are autoimmune

88
Q

Describe the size and infection rate of vegetation

A

the bigger the vegetation then the more likely it is infected as the growth of infecting organisms is added to the growing clot

89
Q

What are the 4 fates of a thrombus?

A
  1. dissolution
  2. propagation
  3. embolization
  4. organization (and recanalization)
90
Q

What is dangerous about catheters and cardiac pacer wires?

A

clot formatino around them is inevitable and carries with it the ever-present dangers of embolization and infection of the clot

the longer the line then the larger and more permanent the clot

91
Q

Describe how organization can occur in pneumonias, exudates, injuries and not just thrombi

A

it is the ingrowth by fibroblasts who convert thrombus to fibrous tissue along with the ingrowth of new capillaries that in turn coalesce to recanalize a thrombosed blood vessel

92
Q

Define embolus. What are the types?

A

a detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin

  1. thrombus (most common)
  2. atheromatous debris
  3. fat
  4. air,
  5. amniotic fluid
  6. fragments of tumor
93
Q

Pulmonary thromboemboli are very common and usually occur from deep vein thrombosis. Describe the size associated disease state

A

Medium sized=> cause hemorrhagic infarction (if bronchial arterial part o fhte dual lung blood supply)

Large size => cause acute cor pulmonale (right heart failure) and sudden death

94
Q

What are “saddle emboli”?

A

in pulmonary trunk and tend to drape of the trunk at autopsy

95
Q

What are paradoxical emboli?

A

they pass through a patent foramen ovale or atrial septal defect to go to organs besides the lungs

very rare

96
Q

Numerous small emboli can cause what?

A

pulmonary hypertension

this is common

97
Q

Describe where you see systemic thromboemboli most commonly (3)

A

heart (80%)

legs (75%)

brain (10%)

98
Q

What is the common cause from long bone fractures? describe the pathology of these and what they may cause. what disease is associated with them?

A

Fat embolism is most commonly from long bone fractures.

Most fat emboli are clinically silent, but large numbers of them can cause a syndrome of sudden onset dyspnea, tachypnea, tachycardia, irritability, restlessness, anemia, and thrombocytopenia.

It usually occurs 1-3 days following trauma.

Sickle cell disease can cause painful bone infarcts and fat embolism from this infarcted bone can be fatal.

99
Q

How is an air embolism caused (3)? what is the seriousness of the pathology?

A

Air embolism can be caused by

  1. getting air into an intravenous infusion,
  2. a sudden change in atmospheric pressure,
  3. chest wall injury or back surgery in a prone position.

Generally more than 100 mL are needed to have any clinical effect, but it can be fatal.

100
Q

What can cause an amniotic fluid embolism? What are the results? What syndrome can this eventually cause?

A

caused by tears in the placental membranes during the course of labor and delivery.

These breaks can result in squamous cells, lanugo hair, vernix caseosa fat and mucin in the pulmonary microcirculation.

A syndrome of sudden severe dyspnea, cyanosis and shock during labor or delivery can be due to amniotic fluid embolism, but this is rare.

101
Q

As in a previous card, An infarct is an area of ischemic necrosis and is usually due to thrombotic or embolic occlusion of an artery. What can less common causes of infarction?

A

much less common causes of infarction.

  1. Vasospasm,
  2. atheroma expansion by intraplaque hemorrhage,
  3. tumor compressing an artery,
  4. twisting of blood vessels (torsion or volvulus),
  5. trauma or an incarcerated hernia are
102
Q

What are “White anemic” infarcts?

A

typical of solid organs with end-arterial circulation (heart, spleen, kidney).

103
Q

What are “red hemorrhagic” infarcts?

A
  1. typical with venous occlusion (as in ovarian torsion),
  2. dual or anastomosing blood supply (in lung or intestines)
  3. with reperfusion.
104
Q

Describe coagulative necrosis wrt to infarction and hemodynamics. What is it in the brain? How is an abscess related?

A

most common histologic form of infarct

usually apparent after 12-18 hours, and usually elicits an acute inflammatory response.

This neutrophilic response peaks at 1-2 days and is followed by macrophages and fibroblasts.

Ischemic necrosis in brain is liquefactive.

Necrotizing infection can abscess.

105
Q

The likelihood of an infarction is determined by what 4 mechanisms?

A

(1) an organ’s vulnerability to hypoxia (neurons die after 4 minutes of ischemia, cardiac myocytes after 20 minutes),
(2) the rate of development of vascular occlusion (if slow, it allows collateral circulation to develop),
(3) the nature of an organ’s blood supply (a dual blood supply is protective, for example, in the liver), and
(4) oxygen content of the blood.

106
Q

To systematically describe an infarct, a hemorrhage, a tumor, basically any lesion, it is helpful to describe five aspects: name them

A

(1) the size of it,
(2) the shape of it,
(3) the color of it,
(4) the consistency [texture] of it (requires palpating the lesion, but the others require only seeing it.)
(5) its relationships [including its location and its proximity to other things].

107
Q

What are the 5 pathophysicologic categories?

A
  1. Increased hydrostatic pressure
  2. Decreased plasma osmotic pressure
  3. Sodium retention
  4. Inflammation
  5. Lymphatic obstruction
108
Q

What is the result of edema in the kidneys? or when a patient suffers from hepatic cirrhosis?

A

Nephrotic syndrome (protein loss)

Hepatic cirrhosis partly due to increased hydrostatic pressure in the portal venous system, but also decreased plasma osmotic pressure due to protein loss into ascites anddeficient hepatic protein synthesis

109
Q

What is this an example of?

A

Lymphedema due to breast cancer

Pathology block 2 (6 decks)

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