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Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

What are considered fluid flow?

A
  • edema
  • hyperemia & congestion
  • hemostasis
  • thrombosis
  • embolism
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2
Q

What are considered vascular disorders?

A
  • hypertension
  • arteriosclerosis
  • aneurysms
  • ischemic heart disease
  • anomalies of heart
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3
Q

What is edema?

A

increased hydrostatic pressure or decreased colloidal osmotic pressure increases fluid movement into tissues

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4
Q

What are the causes of edema?

A
  • increased hydrostatic pressure
  • reduced plasma osmotic pressure
  • lymphatic obstruction
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5
Q

What are the types of edema?

A
  • exudate: high protein content
  • transudate: low protein content
  • subcutaneous: below heart where hydrostatic pressure is high
  • pulmonary: renal failure, CAD, inflammation
  • brain: increased intracranial pressure causes abnormal herniation of brain tissue
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6
Q

What is hyperemia & congestion?

A
  • both: increased blood volume in tissue
  • hyperemia: active increase is blood volume
  • congestion: passive increase blood volume; have cyanosis
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7
Q

What is hemostasis?

A
  • maintaining blood; clot free state
  • vasoconstriction & release endothelin
  • glycoprotein 1B to adhere to ECM vWF
  • promotes platelet aggregation=primary hemostasis
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8
Q

What occurs in platelet adhesion?

A

mediated by Gp1b platelet surface receptor to collagen bound vWF

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9
Q

What occurs in platelet activation & aggregation?

A
  • confromational change
  • secrete thromboxane A2
  • platelet plug stability with fiubrin clot=secondary hemostasis
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10
Q

What occurs duing secondary hemostasis?

A
  • release of tissue factor 3
  • thrombin production
  • fibrin clot
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11
Q

What occurs during antithrombotic counterregulaiton?

A
  • counter regulatory mechanisms
  • plasminogen activator & thrombomodulin
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12
Q

What are the key players in the endothelium pro-thrombotic process?

A
  • tPAI
  • vWF
  • tissue factor 3 thromboplastin
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13
Q

What are the key players in the endothelium anti-thrombotic process?

A
  • NO
  • prostaglandin I2
  • tPA
  • thrombomodulin
  • tissue factor inhibitor, heparin
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14
Q

What is the coagulation cascade?

A
  • product is thrombin to drive fibrin clot
  • co-factor: Ca++
  • intrinsic & extrinsic pathways activate factor X
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15
Q

What is the fibrinolytic system?

A
  • coagulation inhibited by activation of fibrinolytic apthway
  • remodeling of fibrin clot
  • driven by tPA
  • serum plasmin inactivated by alpha 2-anti-plasmin
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16
Q

What are the roles of thrombin in hemostasis?

A
  • platelet aggregation
  • endothelial activation
  • leukocyte activation
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17
Q

What are the chracteristics of hemorrhage?

A
  • characterized by gross morphologic appearance
  • can be internal or external
  • bleeds into cavities-> hemothorax, hemopericardium, hemoperitoneum, hemathrosis (joints)
  • petechiae= 1-2 mm
  • purpura= 3-5 mm
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18
Q

What are ecchymoses and hematomas in hemorrhages?

A
  • eccy: bruises >10mm caused by trauma
  • hema: solid collections of coagulated blood
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19
Q

What are the 4 types of shock?

A
  • cardiogenic: low cardiac output d/t myocardial pump failure
  • hypovolemic: loss of blood or plasma reducing cardiac output
  • anaphylactic: loss of blood/plasma reducing cardiac output d/t vasodilation
  • septic: excessive vasodilation
20
Q

What are the 3 abnormalities that contribute to thrombosis?

A

Virchow’s triad
* endothelial injury
* genetic/acquired conditions
* turbulent blood flow/stasis

21
Q

What are thrombi?

A
  • anywhere in vascular system
  • arterial & cardiac -> endothelial injury
  • mural: heart chambers & aorta
  • arterial: grow in retrograde (opposite of flow)
  • venous: develop at stasis; anti-retrograde (direction of flow)
22
Q

What are the significances of thrombi?

A
  • superficial venous thrombi: rarely embolize, painful, swelling
  • deep vein thromboses: in larger leg veins, embolize to lungs
23
Q

What are the types of systemic embolism?

A
  • fat: from bone fracture
  • amniotic fluid: during labor
  • air: in some surgeries, nitrogen into bloodstream
  • septic: live bacteria; in bacterial endocarditis
  • athero: disruption of atherosclerotic plaque
24
Q

What do infarction and ischemia lead to?

A
  • infarction & ischemia -> coagulative necrosis
  • iscehmic infarcts in CNS -> liquefactive necrosis
  • restored by reperfusion
25
Q

What are red & white infarcts?

A
  • red: venous congestion, loose tissue with space for blood
  • white: arterial in solid organs with end-arterial circulation; wedge shaped
26
Q

What are the clinical impacts of infarction?

A
  1. anatomy of vascular supply
  2. hypoxemia
  3. rate of occlusion
  4. tissue susceptibility to ischemia
27
Q

What is blood pressure?

A
  • cardiac output & vascular resistance
  • renal Na+ excretion/resorption
  • caused by reduced renal Na or increased vascular resistance
28
Q

What is arteriosclerosis?

A
  • small arteries & arterioles in pts with hypertension or diabetes
  • Monckeberg’s: dystrophic calcification of media; does not result in significant luminal narrowing
29
Q

What is hyaline arteriosclerosis?

A
  • diabetes
  • thickened arterial walls by protein deposit
30
Q

What is hyperplastic arteriosclerosis?

A
  • SM cells in media of small arteries (onion like)
  • fibrinoid necrosis
31
Q

What are the constitutional & modifiable risk factors of atherosclerosis?

A
  • constitutional: family genetics, age, male, obesity
  • modifiable: lyperlipidemia, hypertension, smoking, obesity
32
Q

What is the pathogensis of atherosclerosis?

A
  • thick intimal layer depends on endothelial cell injury hemodynamic disturbance, lipids
  • SM cells -> foam cells
  • fatty streak -> early atherosclerotic deposition
  • plaques enlarge -> obstruction to vascular flow
  • hypoxia occurs
33
Q

What are aneurysms?

A
  • true: involve all 3 layers of vessel
  • false: blood leaks completely out of artery or vein
34
Q

What is an abdominal aortic aneurysm?

A
  • b/w renal arteries & aortic bifurcation
  • associated with atherosclerosis
  • vascular occlusions, embolism, rupture, impingement
35
Q

What is a thoracic aortic aneurysm?

A
  • associated with hypertension & Marfan syndrome
  • result fo compression of mediastinal structures
36
Q

What are aortic aneurysms?

A
  • intimal tear
  • results in masive hemorrhage or cardiac tamponade
  • double-barreled aorta
  • end-organ infarction
37
Q

What are the types of aortic dissections?

A
  • type A: ascending aorta (brian damage)
  • type B: descending aorta (brain function is ok)
38
Q

What are the abnormalities of the heart?

A
  1. failure of heart pump -> ischemic heart disease
  2. shunted flow -> patent foramen ovale
  3. regurgitation/obstructed valve flow -> calcific aortic stenosis
  4. disorder of cardiac conduction -> arrythmias
39
Q

What is ischemic heart disease?

A
  • myocardial ischemia
  • results from coronary artery blood flow
  • common clincal syndromes: angina, heart attack, chronic ischemic heart disease
40
Q

What is angina?

A
  • recurrent, reversible myocardial ischemia
  • stable: CP & SOB precipitated by exertion or nitroglycerin
  • unstable: CP & SOB at rest; plaque change; can progress ot transmural heart attack
  • PRinzmetal’s: uncommon; pain at rest d/t coronary vasospasm
41
Q

What are the types of MI tissure injury?

A
  • transmural (full wall thickness)
  • subendocardial more susceptible to damage
42
Q

What are the biomarkers of MI?

A
  • creatin kinase-MB
  • cardiac troponin
43
Q

What is the patent foramen ovale?

A
  • persistent right to left atrial flow
  • hypoxemia
  • increase risk of DVT
44
Q

What is valvar heart disease?

A
  • heart valves lack vasculature
  • bacterial infection
45
Q

What is calcific aortic valve stenosis?

A
  • on older pts
  • calcification
  • left ventricular hypertrophy
46
Q

What does a cardiac conduction require?

A

atrioventricular node, bundle of his, right & left branches

47
Q

What are the stages of a basic ECG?

A
  • P wave: polarization
  • PR interval: conduction is normal
  • QRS: depolarization
  • ST: flat plateau
  • T: repolarization

Pathology (7 decks)

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