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KN-Pathology Block 2 > Hemodynamics 1 - Nichols > Flashcards

Hemodynamics 1 - Nichols Flashcards

1
Q

Does pneumococcus bacteria have capsule? Does staph?

A

yes. Staph does not.

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2
Q

What is required for a diagnosis of SIRS?

A 
any two of these:
hyper or hypothermia
high heart rate
high respiratory
high or low WBC or bandemia

can be from infection or systemic inflammation.

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3
Q

Does the gallbladder often get infected by bacteria and viruses?

A

No.

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4
Q

What do gall stones often require as treatment?

A

cholecystectomy

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5
Q

What is TSS?

A

toxic shock syndrome consists of high fever, shock, diffuse red skin rash and multisystem dysfunction usually due to a staph aureus superantigen that nonspecifically activates many clones of T lymphocytes causing a cytokine storm.

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6
Q

What is edema?

A

generalized swelling of tissue due to increased fluid in interstitial tissue spaces. Can be localized or generalized.

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7
Q

What is the most common cause of edema?

A

heart failure.

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8
Q

What is hydrothorax?

A

fluid in a pleural cavity (pleural effusion).

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9
Q

What is ascites?

A

fluid in the abdominal cavity (peritoneal effusion)

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10
Q

What is anasarca? What can cause it?

A

Generalized edema. Renal failure (only one example)

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11
Q

What is one of the first signs of nephrotic syndrome?

A

periorbital edema (or edema in tissues with loose connective tissue matrix) 99% of the time it is pitting so usually periorbital edema refers to pitting edema.

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12
Q

What are the 5 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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13
Q

What typically causes hydrostatic pressure edema in legs/lower body?

A

deep venous thrombosis or right heart failure

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14
Q

What typically causes hydrostatic pressure edema in the lungs?

A

left heart failure

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15
Q

When would you expect hydrostatic edema in the legs to be worse: recumbant or standing?
What about if it were in the sacrum?

A

worse in legs when standing

worse in sacrum when recumbant (lying down)

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16
Q

What type of edema would you commonly expect with increased hydrostatic pressure?

A

Sodium retention edema
Increased hydrostatic pressure edema can cause decreased renal blood flow, which activates the renin-angiotensisn-aldosterone system. Increased aldosterone causes retention of sodium and water, which causes further edema.

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17
Q

What type of edema is caused by nephrotic syndrome?

A

edema from decreased plasma osmotic pressure. Nephrotic syndrome is due to protein loss through the kidneys.

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18
Q

What protein makes up nearly half of total plasma protein?

A

albumin. It plays a major role in plasma osmotic pressure

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19
Q

What will hypoalbuminemia cause?

A

generalized edemaand secondary hyperaldosteronism, which then causes sodium retention edema

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20
Q

What usually causes edema due to sodium retention?

A

heart or kidney failure

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21
Q

Where is sodium retention edema be localized?

A

sodium retention edema is always generalized throughout body

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22
Q

What can cause edema due to inflammation to become a generalized global event?

A

SIRS or sepsis

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23
Q

What typically causes lymphedema?

A

lymphatic obstruction.

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24
Q

What type of edema generates a “peau d’orange” skin characteristic?

A

lymphedema. Skin begins to resemble an orange peel

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25
Q

What is the most common cause of pulmonary edema? What are some other causes?

A

left heart failure.

acute respiratory distress syndrome (ARDS), hypersensitivity reactions, pneumonia and renal failure.

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26
Q

What is a major symptom/sign of pulmonary edema?

A

dyspnea (shortness of breath) and pulmonary crackles

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27
Q

What makes cerebral edema potentially fatal?

A

herniation of the cerebellar tonsils into the foramen magnum, which compresses the brainstem and suppresses the respiration center

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28
Q

What is hyperemia?

A

erythema. an active increase in arterial blood flow, causing an abnormal reddish coloration due to the presence of excess oxygenated blood in a tissue

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29
Q

What is the most common cause of hyperemia?

A

inflammation

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30
Q

What is congestion?

A

passive decrease in venous outflow. It caues cyanosis (an abnormal bluish coloration due to excess deoxygenated blood)

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31
Q

What pathological states can cause cyanosis?

A

congestion, failure of lungs to load oxygen in blood, cardiovascular or pulmonary diseases, right heart failure.

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32
Q

What is nutmeg liver associated with?

A

passive congestion from right heart failure.

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33
Q

Where is passive congestion the worst?

A

centrilobular areas

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34
Q

What is nutmeg liver?

A

alternating red and tan tissue casuinng the cut surface of the liver to resemble the cut surface of a nutmeg

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35
Q

Can hyperemia or congestion be fatal?

A

Not according to nichols

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36
Q

What would cause accumulation of hemophages in pulmonary alveoli (with iron from blood that has leaked into the alveoli due to capillaries burst from the high pressure)?

A

chronic sublethal left heart failure

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37
Q

What is a hematoma?

A

when a hemorrhage is enclosed within tissue

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38
Q

What are petechiae?

A

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

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39
Q

What are purpura?

A

Medium (3-10 mm) hemorrhages due to vaculitis, vessel fragility, etc

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40
Q

What are Ecchymoses?

A

larger (over 1 cm) subcutaneous hemorrhages that go from red-blue to blue-green to gold=brown as the hemoglobin breaks down.
Frequently called bruises. (bruises do not have to be from trauma)

41
Q

What is a hemopericardium?

A

hemorrhage into the pericardial space

42
Q

What is a hemoperitoneum?

A

hemorrhage inot the abdominal cavity

43
Q

What is a hemoarthrosis?

A

hemorrhage into a joint (commonly associated with hemophilia)

44
Q

What is hemostasis?

A
  1. the maintenance of blood in a free-flowing liquid state in normal blood vessels
  2. the formation of a blood clot at a site of vascular injury
45
Q

What three things regulate hemostasis?

A

vascular wall (endothelium), platelets, and coagulation cascade

46
Q

What do platelets contain?

A

ADP, fibrinogen, clotting factors V and VII, Calcium, and epinephrine

47
Q

What are the four stages of hemostasis at a site of vascular injury?

A
  1. vasoconstriction
  2. primary hemostasis
  3. secondary hemostasis
  4. thrombus and antithrombotic events
48
Q

Which clotting factors do platelets carry?

A

Clotting factor V and VII

49
Q

What happens in Stage 1 of hemostasis?

A

vasoconstriction. There is a brief arteriolar vasoconstriction medicated by reflex neurogenic mechanisms that are augmented by local secretion vasoconstrictors such as endothelin

50
Q

What is endothelin?

A

(potent endothelium derived vasoconstrictor)

51
Q

What happens in stage 2 of hemostasis?

A

Primary hemostasis. Platelet adhesion to thrombogenic extracellular matrix takes place. Platelet adhesion to extracellular matrix is mediated by bon Wilebrand factor, which binds to their GpIb receptors. Platelets change from smooth-surfaced discs to spheres with numerous long spiky projections for aggregation.

52
Q

What binds to GpIb receptors on platelets? What does this do?

A

von Willebrand factor does this to promote binding of platelets to extracellular matrix. It causes a change in platelet shape

53
Q

What two molecules are released after GpIIb/IIIa receptors are activated on platelets?

A

ADP and thromboxane A2 from platelet granules, which causes further platelet recruitment and aggregation.

54
Q

What receptors are asssociated with a conformational change in platelet shape?

A

GpIIb/IIIa

55
Q

What happens in stage 3 hemostasis?

A

secondary hemostasis. The coagulation cascade is activated by tissue factors and platelet factors.

56
Q

What is clotting factor III?

A

tissue clotting factor.

57
Q

What is thromboplastin?

A

a lab reagent that contains phospholipids and tissue clotting factor.

58
Q

What does thrombin do?

A
  1. converts fibrinogen to fibrin
  2. stimulates platelets to release thromboxane A2
  3. activates monocytes and lymphocytes
  4. stimulates endothelial cells to adhere to neutrophils and release NO, tissue plasminogen activator and prostacyclin.
59
Q

What happens in stage 4 hemostasis?

A

thrombus stabilization and antithrombotic events. A solid semi-permanent plug of aggregated platelets and polymerized fibrin is formed. Counter-regulatory mechanisms limit the hemostatic plug to site of injury.

60
Q

What limits hemostatic plugs to sites of injury?

A

thrombomodulin binds thrombin and together they activate protein C, an anti-coagulant.
The fibrinolytic system of t-PA, plasmin, tissue factor pathway inhibitor, antithrombin II, heparin-like molecules, protein S and urokinase also inhibit it.

61
Q

What does deficiency of the von Willebrand factor cause?

A

tendency to bleed excessively with surgery or menstruation (von Willebrand disease).

62
Q

What does overactivity of the von Willebrand factor do?

A

tendency to clot in small blood vessels and then bleed from having used up too many platelets and clotting factors (thrombotic thrombocytopenic purpura)

63
Q

What does deficiency of platelet GpIb receptor do?

A

causes bleeding tendency (Bernard-Soulier syndrome)

64
Q

What does GbIb bind to?

A

von willebrand factor

65
Q

What will a deficiency in GpIIb/IIIa receptors cause?

A

bleeding tendency due to deficient platelet aggregation (Glanzmann thrombasthenia)
Snake venom can do this.

66
Q

What is eptifibatide (integrilin)?

A

anti-coag drug that mimiks snake venom by binding to platelet GpIIb/IIIa receptors.

67
Q

What role does ADP play in hemostasis?

A

induces the conformation change that mediates the binding of platelet GpIIB/IIIa receptors to fibrinogen and other platelets to cause aggregation.

68
Q

What is clopidogrel (plavix)?

A

Blocks platelet ADP receptors.

69
Q

What is thrombosis?

A

inappropriate formation of a blood clot in a blood vessel, usually occlusive

70
Q

What are three predisposing factors for thrombosis?

A
  1. endothelial injury (smoking, hypertension, and hyperlipidemia cause this)
  2. abnormal blood flow
  3. hypercoagulability
71
Q

What effect does turbulant blood flow have on clotting?

A

it promotes it

72
Q

Is thrombosis more common in arteries or veins? Where is it more life-threatening?

A

more common in veins,

more dangerous in arteries

73
Q

What does Factor V Leiden mutation cause?

A

It is an inherited disease that causes hypercoagulability. It makes factor V clotting factor resistant to activated protein-C, resulting in loss of clot-limiting regulation.

74
Q

What will Prothrombin G20210A mutation cause?

A

confers a 3x risk of venous thrombosis

75
Q

What is antiphospholipid antibody syndrome?

A

rare, life-threatening acquired hypercoagulable state. It causes arterial thrombosis. Most common in young females. They have autoantibodies against phospholipids or proteins that bind to them.
They are called lupus anticoagulants.

76
Q

What are thrombi? What are the three different types?

A

blood clots.

arterial thrombi, venous, and mural thrombi

77
Q

Describe arterial thrombi.

A

rich in platelets (white thrombi)

78
Q

Describe venous thrombi.

A

rich in erythrocytes (red thrombi)

79
Q

Describe mural thrombi.

A

Located on wall of heart. Newer clots are more likely to break off and embolize

80
Q

What effect can obesity have on ultrasound diagnosis of deep vein thrombosis?

A

Can cause false negatives

81
Q

What are thrombi on heart valves called?

A

vegetations

82
Q

What is Libman-Sacks endocarditis?

A

Autoimmune vegetation

83
Q

What is marantic endocarditis?

A

Non-bacterial thrombotic endocarditis

84
Q

Are bigger or smaller endocarditises more likely to get infected?

A

bigger ones have greater chance of infection

85
Q

What four things can happen to thrombi?

A
  1. dissolution
  2. propagation
  3. embolization
  4. organization (recanalization)
86
Q

What is organization?

A

ingrowth of by fibroblasts, who convert it to fibrous tissue, with ingrowth of new capillaries who can coalesce to recanalize a thrombosed blood vessel.
higher risk of it the longer a catheter is in, can cause major bleeding if catheter removed.

87
Q

What is an embolism?

A

detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin. Can be thrombus, atheromatous debris, fat, air, amniotic fluid, or fragments of tumors.
80% of them are clinically silent.

88
Q

What are saddle emboli?

A

emboli in the pulmonary trunk that drape over the heart at autopsy

89
Q

What are paradoxical emboli?

A

ones that pass thorugh a patent foramen ovale or arterial septal defect to go to organs besides the lungs

90
Q

What can numerous small emboli cause?

A

pulmonary hypertension. Rather common

91
Q

Where do most systemic thromboemboli form? Where do the usually go?

A

in the heart. Usually go to the legs and brain

92
Q

When do fat embolisms usually occur?

A

after long bone fractures

93
Q

What causes air embolisms?

A

IVs or sudden changes in atmospheric pressure (scuba or planes), chest wall injury or back surgery in a prone position.
usually 100mL to see effects

94
Q

What would cause squamous cells, lanugo hair, vernix caseosa fat and mucin to enter pulmonary circulation?

A

amniotic fluid embolisms caused by tears in placental membranes during course of labor and delivery.

95
Q

Where are white anemic infarcts typical?

A

in solid organs with end-arterial circulation (heart, spleen, kidney)

96
Q

Where are red hemorrhagic infarts typical?

A

with venous occlusion (ovarian or testicular torsion), dual or anastomosing blood supplies (lungs or intestines) or with reperfusion.

97
Q

What is the most common type of infarct?

A

coagulative necrosis.

98
Q

What 5 things are important when describing a lesion?

A
  1. size
  2. shape
  3. color
  4. consistency or texture
  5. location and relationship to other things
99
Q

What is coagulopathy?

A

abnormal tendency to bleed

KN-Pathology Block 2 (10 decks)

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