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FM1- Pathology > Intro to Hemodynamic Disorders > Flashcards

Intro to Hemodynamic Disorders Flashcards

1
Q
  1. Define edema.
A

an increased amount of fluid in the tissue interstitial spaces and potential spaces

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2
Q
  1. Define effusion.
A

accumulation of fluid in a particular body cavity such as pleural effusion or a pericardial effusion

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3
Q
  1. Define ascites.
A

a fluid accumulation in the abdominal cavity

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4
Q
  1. Define anasarca.
A

severe and generalized edema with diffuse involvement of all interstitial tissues with grossly evident diffuse subcutaneous swelling

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5
Q
  1. Define exudate.
A

loss of fluid with proteins from vessel

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6
Q
  1. Define transudate.
A

loss of fluid (without protein and cells) from the vessel

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7
Q
  1. Define chronic passive congestion.
A

generally results from impaired outflow of blood, generally appears darker blue-red due to accumulation of deoxygenation

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8
Q
  1. Define heart failure cells.
A

hemosiderin-laden macrophages in the alveoli and pulmonary interstitial spaces are termed heart failure cells

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9
Q
  1. Define nutmeg liver.
A

a result of passive congestion, noted by discoloration of the liver; back up of capillary beds cause pressure necrosis around hepatic veins

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10
Q
  1. Define cardiac cirrhosis.
A

cirrhosis that is caused by right heart failure causing cetrilobular necrosis due to hypoxic/ischemic injury due to back of blood from the right side of the heart

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11
Q
  1. Define hematoma.
A

blood accumulation in a space or tissue; causes a displacement of tissue, creating pressure

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12
Q
  1. Define contusion, ecchymosis.
A

extraversion of blood into the tissue, often cutaneous or subcutaneous tissue, due to vascular rupture in which is the skin is not broken

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13
Q
  1. Define petechiae.
A

small (1-2mm) punctate hemorrhages usually due to thrombocytopenia and seen on skin or mucosal/serosal surfaces

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14
Q
  1. Define purpura.
A

larger punctate hemorrhages, common with vasculitis, or with low platelets

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15
Q
  1. Define saddle embolus.
A

really large pulmonary thromboembolism which occludes right and left pulmonary arteries

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16
Q
  1. Define paradoxical embolus.
A

a venous thromboembolus passing through an atrial or ventricular heart defect to lodge in the systemic arterial system

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17
Q
  1. List 5 major pathophysiologic categories of edema.
A
  1. increased hydrostatic pressure/impaired venous return
  2. reduced plasma oncotic pressure
  3. lymphatic obstruction
  4. sodium retention
  5. inflammation
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18
Q

(6) Compare and contrast hyperemia and congestion

A

both describe local increase in blood volume, hyperemia as in active arteriolar dilation occurs naturally in exercise (appears more red) while congestion is a result of the outflow of capillary beds getting is obstructed (appear more cyanotic)

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19
Q
  1. What is hemorrhage?
A

extravasation of blood due to vessel rupture as in vascular injury or injury coupled with disease or neoplasia

20
Q
  1. Hemostasis requires three components…
A

vascular wall
platelets
coagulation proteins

21
Q
  1. Name the major steps of hemostasis. (~3)
A
  1. arteriolar vasoconstriction
  2. platelet adherence, activation and aggregation (primary hemostasis)
  3. generation of thrombin and fibrin with polymerization of fibrin and platelet aggregates (secondary hemostasis)
22
Q
  1. Describe the molecules that are involved in primary hemostasis.
A
  1. collagen is exposed to blood von Wilebrand F and bind together
  2. platelets bind to vWF factor via a Gp1b
    binding of platelets causes flattening and release of granules
23
Q
  1. Describe the molecules of secondary hemostasis.
A
  1. endothelial cells release tissue factor, which initiates the clotting cascade- activation of thrombin
  2. thrombin cleaves fibrinogen to fibrin which can polymerize
24
Q
  1. What is thrombosis?
A

pathologic activation of hemostatic mechanism (clot occurs inside blood vessel without disruption)

25
Q
  1. What are the three parts of the Virchow triad.
A
  1. endothelial injury (interruption of endothelium)
  2. abnormal blood flow (due to stasis or turbulence)
  3. hyper-coagulability
26
Q
  1. Differentiate between abnormal blood flow patterns that usually contribute to venous v. arterial thrombosis.
A

arterial- turbulent flow

venous- stasis

27
Q
  1. Differentiate between primary and secondary hyper coagulable state and I’ve examples of each.
A

primary/genetic: factor V Leiden, prothrombin mutation

secondary/acquired: visceral malignancy, hyperestrogenic states (pregnancy, oral contraceptive)

28
Q
  1. Describe the four possible outcomes of thrombosis.
A
  1. propagation of thrombus
  2. repair and wound healing causes organized reanalyzed
  3. clots organized and incorporated into a cell wall
  4. complete resolution of the clot
  5. clot can cause embolus to travel to the lung
29
Q
  1. Differentiate between thrombus, embolus and thromboembolus.
A

thrombus is a clot that stays where it occurs, where an embolus can be a solid, liquid or gaseous mass that travel to a distant site; a thromboembolus is an embolus made of thromboses blood

30
Q
  1. Describe pulmonary thromboembolism with respect to pathogenesis, risk factors and clinical outcome.
A

95% of these originate in the deep venous system of the lower limbs called DVT, it is the most common type of embolism, consider also a air embolism caused by trauma or complicated births

31
Q
  1. Contrast venous and arterial thromboembolism.
A

venous embolism usually lodges in the lung while an arterial embolism is more likely to cause infarction

32
Q
  1. Give two mechanisms for infarction and distinguish between red and white infarcts.
A

mechanisms: arterial thrombosis or thromboembolism, red infarcts are caused when blood flow is restored after tissue death, white infarcts is tissue death without resumption of blood flow

33
Q
  1. Describe four major factors influencing the development of an infarct.
A

nature of vascular supply (dual v. end-arterial)
rate of occlusion of vascular supply
susceptibility of tissue to infarction
oxygen of content of blood

34
Q
  1. Describe the three major types of shock.
A

cardiogenic: failure of pump (cardiac infarction, cardiac tamponade)
hypovolemic: substantial loss of intravascular volume (burns, diarrhea, vomiting, dehydration)
septic: wide spread connotation of widespread infection with severe systemic inflammation (most popular gram-positive bacteria)

35
Q
  1. How do gram negative bacteria trigger septic shock?
A

lipopolysaccharides= LPS= endotoxin released when inflammatory response lyses bacteria

36
Q
  1. Describe the events that lead up to the profound hypotension due to sepsis.
A

microbial produces cause reaction of neutrophils and macrophages

release of cytokines and mediators cause endothelial cells to cause as systemic vasodilation and profound dilation

37
Q
  1. List 3 major complication so septic shock.
A

acute reparatory distress
diffuse alveolar disease
disseminated intravascular coagulation

38
Q
  1. Describe acute respiratory distress.
A

(ARDS) is a clinical syndrome of pulmonary dysfunction caused by a diffuse alveolar capillary damage;

39
Q
  1. Describe diffuse alveolar disease.
A

(DAD) describes the histology of the lung pathoneumonic fixing of hyaline membranes caused by fluid and fibrin leaking into the pulmonary interstitial and alveoli (associated with ARDS)

40
Q
  1. What is disseminated intravascular coagulation.
A

widespread activation of coagulation within blood vessels and is characterized by consumption of coagulation factors as well as widespread activation of fibrinolytic system which leads to excessive bleeding

41
Q
  1. List two specific independent mechanisms by which hepatic cirrhosis and liver failure can generate edema
A

lack of production of plasma proteins and chronic passive congestion

42
Q

Platelet aggregation is mediated by platelet receptor _______.

A

GpIIb-IIIa.

43
Q

Name two non-thromboembolic infarcts.

A

twisting of a loop of the intestine (volvulus) or similarly testicular or ovarian torsion

44
Q

How long a period of hypoxia before neurons and cardiomyocytes show damage?

A

3-5 min for neurons and 30min for myocytes

45
Q

What are the signs of multi system organ failure?

A

hypoxemia/ acidosis (2ary to necrosis and ARDS) oliguria/anuria (tubular necrosis) and confusion (hypoxia to brain)

considered a terminal complication in fatal cases of septic shock

FM1- Pathology (6 decks)

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