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Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

5 Major Categories of Edema

A
  1. Increased hydrostatic pressure / impaired venous return
  2. Reduced plasma oncotic pressure (hypoproteinemia)
  3. Lymphatic obstruction • generally a long term obstruction not a few minutes
  4. Sodium retention
    - increases hydrostatic pressure and decreases osmotic pressure
  5. Inflammation
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2
Q

Hyperemia vs. Congestion

A

Both terms describe local increase in blood volume

1) hyperemia
- active process
- arteriolar dilation
- erythema

2) Congestion
- passive process -
- impaired outflow -
- cyanotic (blue/red)

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3
Q

Liver with Chronic Passive Congestion

A

Results from long standing congestion w/resulting hypoxia and cellular or tissue degradation

If persistent and severe, can be fibrosis and necrosis

-centrilobular congestion

Often due to right sided heart failure thus cardia cirrhosis

“Nutmeg Liver”

Brown: around central vein which is experiencing congestion

Tan: Around portal triad which is okay due to dual blood supply

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4
Q

Heart Failure Cells

A

Hemosiderin-laden macrophages in the alveoli and pulmonary interstitial spaces found in pulmonary congestion which is most often due to LEFT sided heart failure

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5
Q
  1. Example of edema due to increases hydrostatic pressure

2. Due to decreased osmotic pressure

A
  1. HP: congestive heart failure leading to pulmonary edema

2. Nephrotic syndrome in which albumin is loss through damaged glomerular capillaries

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6
Q

Two mechanisms by which cirrhosis/liver failure can cause edema

A
  1. Hypoproteinemia

2. Vascular obstruction backing up into portal circulation causing ascites

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7
Q

Exudate vs. transudate

A
  1. Exudate
    - Protein rich fluid with a specific gravity>1.020
  2. Transudate
    - clear serous fluid
    - low protein content
    - SG
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8
Q

Hemorrhage

A

■ Extravasation of blood due to vessel rupture

■ Causes
– vascular injury (trauma)
– vascular disease (e.g., atherosclerosis, inflammation, neoplasia) +/- minor trauma
– defects in clotting mechanism + minor
trauma
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9
Q

Hematoma

A

blood accumulation in a space or tissue

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10
Q

Petechiae

A

Petechiae: small (1-2 mm) punctate hemorrhages
– seen on skin or mucosal/serosal surfaces
– low platelets (thrombocytopenia)

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11
Q

Purpura

A

■ Purpura: slightly larger (≥ 3 mm)
– low platelets
– small vessel vasculitis

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12
Q

Hemostasis

A

■ Rapid formation of a localized plug at site of vascular disruption

■ Requires three components to interact
– vascular wall (especially endothelium)
– platelets
– coagulation proteins

***Major Events***
■ Arteriolar vasoconstriction
■ Platelet adherence, activation and
aggregation (primary hemostasis)
■ Generation of thrombin and fibrin with
polymerization of fibrin and platelet
aggregates (secondary hemostasis)
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13
Q

Primary Hemostasis

A
  1. Platelet Adhesion
    - platelets adhere to endothelia vWF via platelet receptor GpIb
  2. Activation
    a) Shape Change
    b) Granule Release
    • ADP, TxA2
  3. Recruitment: ADP/TxA2 attract more platelets
  4. Aggregation
    - via platelet receptor GpIIb-IIIa binding to fibrinogen

RESULT: Platelet Plug

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14
Q

Secondary Hemostasis

A

Basically activation of the coagulation cascade

  1. Tissue Factor (Factor III/thromboplastin)
  2. Phospholipid complex expression
  3. Thrombin activation
    - coagulation cascade activates thrombin from prothrombin
  4. Fibrin polymerization
    - thrombin cleaves fibrinogen into fibrin
    - fibrin now makes a meshwork
    - Remember that fibrinogen was holding platelets together
    - thrombin also recruits more platelets

RESULT: more permanent hemostatic plug

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15
Q

Thrombosis

A

Pathologic activation of hemostatic mechanism (clot occurs inside blood vessel)

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16
Q

Virchow Triad

A

Predisposes to thrombosis

  1. Endothelial Injury (biggest factor)
  2. Abnormal blood flow (2nd most)
  3. Hypercoagulability
17
Q

Venous vs. Arterial thrombosis and thromboemoblism

A
  1. venous-stasis
    - immobility
    - DVTs in legs
    - venous thromboemboli travel downstream since veins are larger they do not initially lodge
    - often enter heart via IVC and exit right ventricle and get lodged in pulmonary vasculature
  2. arterial-turbulent flow
    - allows platelets in aggregate in blood
    - seen in aneurysms and atherosclerotic plaques
  • atrial fibrillation*
  • left atria: stroke or peripheral vascular obstruction

arterial thromboembolism: TE’s get lodged as they travel down, because arteries get smaller as they move away from the heart
-ultimately causes vascular occlusion, tissue ischemia, and potential infarction

18
Q

Hypercoagulability

  1. Primary
  2. Secondary
A

Either hyperactive coagulation or relative inactivity of anticoagulation

  1. genetic
    ■ factor V Leiden mutation (activated protein C resistance)
    -factor V won’t cleave which is necessary for anticoagulation

■ prothrombin mutation
-increased levels of prothrombin
■ others

2.acquired
■ visceral malignancy (Trousseau’s syndrome)
• neoplasia produces coag proteins and causes clots to form randomly
■ hyperestrogenic states (pregnancy, oral contraceptive pills)
■ others

19
Q

Potential Fates of Thrombus

A
  1. Propagation
  2. Resolution/dissolution via fibrinolytic activity
  3. Embolizaton
  4. Organized and Recanalized or just organized into a wall
    - Shows that thrombus formed a long time ago
20
Q

Embolus

A

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

21
Q

Ecchymosis, Contusion, bruise

A

Extravasation of blood into tissue due to traumatic vascular rupture in which skin is not broken

  • Ec-Skin discoloration due to blood leaking into tissue
  • similar to purpura
22
Q

■ Pulmonary thromboembolism (PE)

A

– most common type of embolism
– over 95% of these originate in the deep venous system of the lower limbs; called deep venous thrombosis (DVT)

  • small thromboemboli can be dealt with via lung’s fibrinolytic activty
  • infarct often avoided due to dual blood supply to the lungs

Risk Factors: Same for DVTS

  • immobility
  • hypercoagulability
  • obesity
23
Q

Saddle Embolus

A

Straddles bifurcation of the pulmonary artery can result in complete right ventricular outflow obstruction

Rapidly fatal

24
Q

Paradoxical embolism

A

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

*started in the veins but skipped lungs and ended in arterial vasculature

25
Q

Infarct

A

an area of ischemic necrosis caused by occlusion of arterial supply or venous drainage
– nearly all result from arterial thrombosis or thromboembolism
**
■ Factors that influence development:

a) nature of vascular supply
■ dual
– lung: pulmonary and bronchial – liver: mesenteric and portal
■ end-arterial

b) rate of occlusion of vascular supply
■ chronic hypoxia induces angiogenesis and neovascularization, which provide alternate pathways for blood flow (collateral circulation)

c) O2 content of the blood
d) Susceptibility of tissue to infarction

26
Q

Red Hemorrhagic infarct

A
  • in several tissues like those with dual blood supply (lung, liver)
  • venous outflow obstruction causing congestion (ovarian torsion)
  • as blood is restored after infarct
27
Q

White anemic infarct

A

-solid organs with end-arterial circulation

28
Q

Susceptibility of tissue to infarction

A
  1. High
    - Neuron (3-5 min)

2. Intermediate (30min-2hrs)

  • Cardiac myocyte
  • Hepatocyte
  • Renal tubular cell
  1. Low (many hrs)
    - Fibroblast
    - Epidermal keratinocyte
    - Skeletal myocyte
29
Q

Histology of infarct

A

Ischemic coagulative necrosis

When completely healed (weeks-months), fibrotic tissue with scattered chronic inflammatory cells and some residual and new vessels

30
Q

Shock and its 3 categories

A

Cardiovascular collapse resulting in
systemic hypoperfusion

■ Three general categories
– hypovolemic
– cardiogenic
– septic

31
Q

Hypovolemic

A

Low Cardiac output

Substantial loss of intravascular volume (about 20-25% reduction)
– hemorrhage
– plasma loss
■ burns
■ diarrhea
■ vomiting
■ dehydration

80-90% otherwise healthy people survive

32
Q

Cardiogenic Shock

A

Low cardiac output

■ Failure of pump
– myocardial infarction (intrinsic damage to heart)
– cardiac tamponade (external compression)
-saddle embolus (outflow obstruction)

*mortality rate ~75%

33
Q

Septic Shock

A

Initially normal or high cardiac output because the same molecules that lead to sepsis can increase cardiac contractility and CO

*Today, most common organisms causing septic shock are Gram-positive bacteria

E. coliLPS endotoxin from gram-negative bacteria

Mechanism:

  1. microbial products activate PMNs and macros
  2. release cytokines and mediators
  3. cause endothelial cells to vasodilate
  4. system wide this causes profound hypoperfusion

Slide 59 for more detail

*mortality rate ~75%

34
Q

Sepsis

A

■ Sepsis: presence of various pus- forming or other pathogenic organisms, or their toxins, in the blood or tissues
■ carries a connotation of widespread infection with systemic inflammatory response—if severe enough, resulting in septic shock

35
Q

Shock: multi-organ system failure

Slide 63

A

Widespread infection–>septic shock

systemic vasodilation–>hypotension–>diffuse hypoperfusion–>ischemia–>multi-system organ failure

36
Q

Shock: disseminated intravascular coagulation (DIC)

A

Widespread activation of both thrombotic (leads to platelet fibrin microthrombi) and antithrombotic mechanisms

  • ***potential hemorrhagic diasthesis due to
  • consumptive coagulopathy
  • activatin of antithrombotic mechanisms
37
Q

Shock: acute respiratory distress syndrome (ARDS)/diffuse alveolar damage (DAD)

A
  1. Acute Respiratory Distress (ARDS), or “Shock Lung”:
    - clinical syndrome of pulmonary dysfunction caused by diffuse alveolar capillary damage

■ Diffuse Alveolar Disease (DAD): the histologic picture of the lung that accompanies the clinical syndrome of ARDS
-gas exchange is severely limited due to hyaline membranes (composed of fibrin-rich protein from leaky alveolar capillaries) Slide 60

Pathology (5 decks)

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