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Pathology > 7. Hemodynamics > Flashcards

7. Hemodynamics Flashcards

1
Q

Describe an amniotic fluid embolism?

A

entry of amniotic fluid containing cells and debris into the maternal circulation through open uterine and cervical veins

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2
Q

When does amniotic fluid embolism normally occur?

A

At the end of labor when the pulmonary emboli are composed of the epithelial constituents (squamae) contained in amniotic fluid.

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3
Q

What are some acute clinical symptom of a mother that gives birth to a fetus with an amniotic fluid embolism?

A

Shortness of breath, cyanosis, and shock that is fatal and can lead to coma and death

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4
Q

What are some secondary risks predisposed by a mother that gives birth to a fetus with an amniotic fluid embolism?

A

A mother who survives the acute episode caused by amniotic fluid embolism is at risk for developing acute respiratory distress syndrome. Se also may die of Disseminated Intravascular Coagulation, a thrombotic microangiopathy.

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5
Q

What is the pathogenesis of DIC?

A

Disseminated Intravascular Coagulation forms from Fibrin thrombi that form in small blood vessels because of uncontrollable coagulopathy, which consumes fibrin and other coagulation factors. Once coagulation factors are depleted, uncontrollable hemorrhage ensues.

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6
Q

Chronic Heart Failure leads to increase of blood volume where in the body? What is the cause?

A

A generalized increase in venous pressure , often due to chronic heart failure, increases blood volume in many organs. This is known as Chronic Passive Congestion.

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7
Q

What organ is most vulnerable to Chronic Passive Failure and why? What is expected clinical manifestation? Histological finding?

A

The LIVER because the Hepatic Veins empty into the Vena Cava immediately INFERIOR to the HEART. PE : hepatomegaly Histology: Sinusoid Dilation and dark foci of centrilobular hepatocyte congestion

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8
Q

What PE finding, upon auscultation, would indicate fluid in the pleural spaces?

A

Bubbly Rales

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9
Q

How does increased pressure effect sinusoids and centrilobular hepatocytes?

A

It leads to sinusoid dilation and pressure atrophy of the centrilobular hepatocytes.

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10
Q

What disease forms a nutmeg liver?

A

Chronic Passive Congestion

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11
Q

What cellular pathology can develop from longstanding passive congestion?

A

Fibrosis. Only in the most extreme cases is the fibrosis sufficiently sever e to justify the label cardiac cirrhosis.

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12
Q

What is Melena? What is it a symptom of?

A

Melena is Black Stool and it is a symptom of upper GI bleeding.

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13
Q

What is the pathogenesis of Melena?

A

blood from ruptured esophageal varices r a peptic ulcer is partially digested by Hydrochloric Acid. Hemoglobin is transformed into a black pigment.

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14
Q

What term describes the black pigment “coffee-grounds” seen in melena?

A

Hematin

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15
Q

What is Hematobilia?

A

Bleeding into the biliary passages as a complication of trauma or neoplasia.

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16
Q

What is Hematochezia?

A

Passage of bloody stools caused by lower gastrointestinal hemorrhage

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17
Q

Peptic Ulcer Disease and Pancreatic Disease will cause what effect on stools?

A

These diseases can cause steatorrhea, the passage of fatty stools

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18
Q

What three factors can lead to both venous and arterial thrombosis?

A

Endothelial injury, stasis, and a hypercoaguble state

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19
Q

Where do most venous thromboses occur?

A

Deep veins of the legs

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20
Q

If a patient is immobilized such as a cervical traction, what is the most likely risk factor for deep venous thrombosis?

A

Stasis

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21
Q

What term refers to bleeding into the joint cavity? What clinical finding would be expected?

A

Hemarthrosis. It is associated with joint swelling. If repeated bleeding occurs, deformities may arise and the joint mobility may be limited

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22
Q

What complication of hempohilia can lead to deformities?

A

Hemarthrosis. It is associated with joint swelling. If repeated bleeding occurs, deformities may arise and the joint mobility may be limited

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23
Q

What is Hematocephalus?

A

An intracranial infusion of blood.

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24
Q

What are possible causes of Hypovolemic shock?

A

Hemorrhage, Fluid Loss from Severe Burns, Diarrhea, Excessive Urine Formation, Perspiration Trauma

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25
Q

How does vascular permeability change in cases of burns or trauma?

A

Direct damage to the microcirculation increases vascular permeability. Individuals with third-degree burns weep large amounts of plasma

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26
Q

What is another name for Chronic Passive Congestion?

A

Passive Hyperemia

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27
Q

Why is passive hyperemia confined to a limb or organ at times/.

A

As a result of localized obstruction to venous drainage.

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28
Q

What are three pathologic findings present in Budd-Chiari Syndrome?

A

Deep venous thrombosis of the leg veins, with resulting edema o f the lower extremity , and thrombosis of the hepatic veins

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29
Q

What is the clinical description of a black eye? Its pattern?

A

Confluent bluish hemorrhage in the skin around the eye. Ecchymosis is a larger superficial hemorrhage in the skin. Following hemorrhage, the initially purple discoloration of the skin turns green and then yellow before resolving.

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30
Q

What is the pathogenesis of ecchymosis?

A

Bilirubin released from the hemoglobin of degraded RBCs are progressively oxidized

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31
Q

Pin Point hemorrhages are also known as ___

A

Petechiae

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32
Q

Where are Pin point hemorrhages usually found?

A

In the skin or conjunctiva.

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33
Q

What is a Purpura?

A

A diffuse superficial hemorrhage in the skin up to 1 cm in diameter.

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34
Q

What is Erythema?

A

redness of the skin or mucous membranes, caused by hyperemia of superficial capillaries

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35
Q

What is Hyperemia?

A

Increase of blood flow tissues due to vaso dilation of precapillary arterioles

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36
Q

What are symptoms of arterial thromboembolism?

A

Sudden pain, absence of pulses, and a cold limb (that must be amputated in some cases)

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37
Q

What are clinical manifestations of ruptured aortic aneurysm?

A

Pain, shock, and a pulsatile mass in the abdomen.

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38
Q

How does CHF effect the lungs?

A

`- Impedes the exit of blood from the lungs, leading to chronic passive congestion in the lungs. Pressure in the alveolar capillaries increase and the vessels become engorged with blood. Microhemorrhages release RBCs into the alveolar spaces, where they are degraded by alveolar macrophages.

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39
Q

What is the effect of left ventricular failure in the lungs?

A

The lungs become congested because blood leaks from the congested pulmonary capillaries into the alveoli.

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40
Q

What are heart failure cells?

A

Alveolar macrophages degrade RBCs and Iron is released and accumulates in the form of hemosiderin which remains in the macrophages. This disease process is often seen in left ventricular heart failure.

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41
Q

What kind of exudate is seen in bacterial pneumonia? virulent pneumonitis?

A

Purulent; Lymphocytic interstitial pneumonitis

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42
Q

What kind of lesions are often seen in patient s with pulmonary hypertension?

A

Plexiform Lesions

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43
Q

Does sepsis lead to hypotension or hypertension?

A

Hypotension

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44
Q

Fever, Tachycardia, Tachypnea, Leukocytosis or Leukopenia is a sign of what systemic response?

A

Systemic Inflammation

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45
Q

What’s the most common cause of septic shock?

A

Gram Negative Organisms

46
Q

Anaphylactic shock is a consequence of what type of reaction?

A

Type I Hypersensitivity

47
Q

What shock is indicative of advanced heart failure? Blood Loss?

A

Cardiogenic Shock; Hypovolemic Shock

48
Q

Neurogenic shock can follow acute injury to the brain or spinal cord. What effect does this have on neural control of vasomotor tone?

A

It leads to generalized vasodilation

49
Q

What brain part is susceptible to infarction due to post partum bleeding?

A

Pituitary because it is enlarged during pregnancy. It is infarcted and this is known as Sheehan Syndrome

50
Q

What can lead to pericardial fluid accumulation?

A

Hemorrhage caused by a ruptured myocardial infarct, dissecting aortic aneurysm, or trauma

51
Q

What is cardiac tamponade?

A

When filling pressure of the heart is exceeded by pressure in the pericardial cavity

52
Q

What is electromechanical dissociation? What is the most common cause of this process?

A

A heart rhythm that should produce a pulse but does not. This is most commonly caused by hypoxemia- a decline in cardiac output

53
Q

What is the most common pathogenic cause of aortic aneurysm?

A

A weakening of the aortic media- cystic medial necrosis. Most patients have a history of hypertension.

54
Q

Widespread ischemic changes secondary to microvascular thrombi is known as what term?

A

Disseminated intravascular coagulation

55
Q

What is passive hyperemia?

A

engorgement of an organ with venous blood

56
Q

What is the pathogenesis of esophageal varices in a patient with alcoholic cirrhosis? What causes fatality in these patients?

A

A patient with cirrhosis has portal hypertension which is increased hydrostatic pressure. Massive hematemesis is a frequent cause of death in patients with esophageal varices.

57
Q

What is the pathogenesis of ascites in a patient with alcoholic cirrhosis?

A

A patient with cirrhosis has decreased intravascular oncotic pressure that leads to ascites

58
Q

What disease is often the cause o f a patient who appears to be on the way to recovery but dies suddenly?

A

Pulmonary Embolism, especially a saddle embolus - a large pulmonary embolus that may lodge at the bifurcation of the main pulmonary artery , obstructing blood flow to both lungs.

59
Q

What occurs if more than half of the pulmonary arterial tree is obstructed in a patient?

A

Severe hypotension that may cause death within minutes.

60
Q

Bacterial endocarditis, paradoxical embolization, and Right ventricular mural thrombus are indicative or VENOUS or ARTERIAL thromboembolism?

A

Arterial

61
Q

Describe the pathway of a paradoxical emboli?

A

They arise in the systemic venous circulation, they then bypass the lungs by traveling through an incompletely closed foramen ovale, they enter the left side of heart, and next block flow to the systemic arterial circulation

62
Q

What type of shunt is a paradoxical emboli most likely seen in?

A

Right to Left because the left arterial pressure is greater than the right.

63
Q

What organs are most susceptible to arterial thromboli?

A

Brain, kidney, heart (LV), lower extremities, Small Intestines, Spleen, Retina

64
Q

What causes Cardiogenic shock?

A

Myocardial pump failure due to Myocardial Infarction or Myocarditis “Obstructive”Shock- conditions that prevent right or left heart filling causing a reduced CO (Ex. Pulm. Embolism, Cardiac Tamponade, and rarely Myxoma)

65
Q

Renal Artery occlusion leads to renal failure. What is the likely cause?

A

Severe atherosclerosis can lead to embolization of atheromatous debris into the renal arteries and vascular tree

66
Q

PE findings, Cardiomegaly, Rales, Orthopnea, Hepatosplenomegaly, Obesity with Pitting Leg Edema together is indicative of what disease process?

A

Pulmonary Edema

67
Q

The rales heard in a patient suffering from CHF with pulmonary edema is caused by what pathology?

A

Expansion of fluid-filled alveoli

68
Q

Right-sided heart failure is often seen with what symptoms?

A

Edema of the lower extremities and hepatosplenomegaly

69
Q

Left-sided heart failure is often seen with what symptoms?

A

Dyspnea, Orthopnea, Paroxysmal Nocturnal Dyspnea, Distended jugular veins.

70
Q

What is the most common cause of mural thrombi in the left ventricle? Effect?

A

Myocardial Infarction; arterial thromboemboli

71
Q

What is a Stroke?

A

Cerebral Infarct

72
Q

Atrial fibrillation can predispose a person to the formation of what kind of emboli?

A

Mural Thrombi

73
Q

What is Marantic Endocarditis?

A

It is also known as Non-bacterial Endocarditis, sterile platelet-fibrin vegetations on leaflets of structurally normal cardiac valves.

74
Q

How does bacterial endocarditis differ from non-bacterial endocarditis?

A

Bacterial endocarditis shows destructive vegetations that erode through the free margins of the valve leaflets while non-bacterial endocarditis shows structurally normal cardiac valves.

75
Q

Myocarditis, Inflammation of the myocardium, is associated with what pathology in myocytes?

A

Necrosis and Degeneration of myocytes

76
Q

What are the 5 possible outcomes of an arterial thrombi?

A
  1. Lysis 2. Propagation 3. Organization 4. Carnalization 5. Embolization
77
Q

Describe Organization

A

Invasion of connective tissue elements including fibroblasts and collagen, which causes a thrombus to become firm and appear grayish white.

78
Q

Describe Canalization

A

The process by which new lamina lined by endothelial cells form within an organized thrombus

79
Q

An increase in size in regards to a thrombus is known as _____

A

Propagation

80
Q

What are Lines of Zahn?

A

Pattern of fibrin and platelets (Can be seen in a thrombus from an aortic aneurysm)

81
Q

What is the most common primary tumor of the heart?

A

Cardiac Myxoma (A benign mesenchymal tumor of the Left Atrium)

82
Q

How can myxoma kill a patient suddenly?

A

Blockage of the mitral valve orifice

83
Q

What is a common secondary pathological process that occurs in patients affected by cardiac myxoma?

A

Arterial embolism and subsequent Stroke

84
Q

Lymphedema is most likely cause by what in the clinical setting?

A

Surgical Removal of Lymph nodes or Tumor Obstruction which causes an obstruction of lymphatic flow.

85
Q

What is lymphangiectasia?

A

Progressive Dilation of lymphatic vessels

86
Q

What can prolonged obstruction of lymph vessels cause?

A

Edema , Lymphangiectasia, and overgrowth of fibrous tissue., and limphangiosarcoma has also been described

87
Q

What is Chyothorax?

A

An accumulation of lymphedema in the pleural space?

88
Q

What body defense ar exudates associated with?

A

Exudates

89
Q

Chronic left ventricular failure leads to what pathology?

A

It impedes blood flow out of the lungs and leads to passive pulmonary congestion (Increased hydrostatic P in alveolar capillaries). Increased pressure forces fluid from the blood into alveolar spaces, resulting in pulmonary edema, which interferes with gas exchange.

90
Q

In patients with CHF, what leads to accumulation of a transudate in the alveoli?

A

Venous engorgement of the lungs. Alveolar capillaries also become engorged with blood.

91
Q

What is Torsion?

A

Torsion is also known as Volvulus. It is most commonly a congenital anomality that is characterized by the interruption of blood supply in the bowel due to the twisting of the bowel over its mesentery

92
Q

What can defective internal rotation during the fetal period cause?

A

Abnormal position of the SI and Colon, anomalous attachments and bands. Explicitly, severe abnormalities include SI and LI volvulus and incarceration of the bowel in an internal hernia. Also undue mobility of the bowel loops.

93
Q

What term refers to the cecum or right colon being invested with a mesentary rather than being retroperitoneal?

A

Cecal Volvulus

94
Q

What can cause a sigmoid volvulus? What is a common clinical symptom?

A

An abnormally long colon; Idiopathic constipation

95
Q

n________in babies with CF, may often be complicated by volvulus and intestinal ___________

A

Meconium Ileus; Atresia

96
Q

What is Meconium Ileus and its cause?

A

Meconium is the intestinal contents that have accumulated in utero. Normally, an infant passes the meconium shortly after birth. Meconium Ileus is small bowel obstruction in the newborn. It is caused by failure to pass the meconium immediately in the post-partum period. In CF , specifically, this is caused by the failure of pancreatic secretions to digest the meconium.

97
Q

A myocardial infarct is structurally described as ______ or ________

A

Transmural (through the entire wall) or Subendocardial

98
Q

What causes a transmural MI?

A

Complete occlusion of a major extramural coronary artery.

99
Q

What is a likely pathogenesis of a subendocardial MI?

A

Prolonged Ischemia caused by partially occluding lesions of the coronary arteries when the requirements of oxygen exceeds the supply (Such as in Shock, Anoxia, or Severe tachycardia)

100
Q

Are thrombotic occlusion more likely to cause transmural or subendocardial infarctions?

A

Transmural

101
Q

What are the two determinants of the gross and microscopic appearance of an infarct?

A

Its location and age

102
Q

How are red infarcts distinguished from pale infarcts?

A

Red infarcts have associated bleeding into the necrotic area from adjacent arteries and veins. Grossly, they are sharply circumscribed, firm, and dark red to purple.

103
Q

Where are pale infarcts typically seen?

A

Heart, Kidneys, Spleen

104
Q

Can red infarcts result from arterial occlusion? Venous Occlusion?

A

Yes, Yes. They can result from either.

105
Q

How does a red infract develop in the heart?

A

When the infracted area is reperfused, as may occur following spontaneous or therapeutically induced lysis of the occluding thrombus.

106
Q

What happens to a red infarct over a period of several days?

A

Acute inflammatory cells infiltrate the necrotic area from the viable border. The cellular debris is phagocytosed and digested by PMN leukocytes and later by macrophages. Granulation tissue eventually forms, to be replaced ultimately by a scar.

107
Q

A pulmonary infarct can be caused by hemorrhage from what arteries?

A

Bronchial arteries.

108
Q

How does Respiratory Distress Syndrome affect alveoli?

A

Lack of surfactant causes higher surface tension at the alveoli at low lung volumes and collapse of the alveoli during expiration

109
Q

What is atelectasis? In a surfactant deficiency, what is the effect on alveoli?

A

Collapse. In surfactant deficiency, collapse of the alveoli occur and there is a perfused but not ventilated alveoli, a situation that leads to hypoxia and acidosis.

110
Q

What is a major complication of Resp. Distress syndrome?

A

intraventricular cerebral hemorrhage because the periventricular germinal matrix in the newborn brain is vulnerable- the veins in this area are dilated and thin and can rupture easily.

111
Q

What is the pathogenesis of brain hemorrhage in a newborn suffering from RDS?

A

Anoxic injury to the periventricular capillaries, venous sludging and thrombosis, and impaired vascular autoregulation.

Pathology (30 decks)

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