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CMOD-Block 2 Path > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

What 3 general pathologic processes lead to edema?

A
  1. Altered Endothelial Function
  2. Increased Vascular Pressure
  3. Decreased Plasma Protein Content
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2
Q

What 3 major causes of morbidity and mortality in developed countries result from thromboembolism?

A
  1. Mycocardial Infarction
  2. Pulmonary Embolism
  3. Cerebrovascular Accident
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3
Q

What is hemostatis and what are its 4 phases?

A

Hemorrhage
Hypotension
Shock
Death

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4
Q

Differentiate between Hemorrhage and Hypotension.

A

Hemorrhage
- Slower Loss of Blood

Hypotension
- Usually results from a massive loss of blood (multiple leaders)

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5
Q

Thrombosis vs. Embolism

- what substrates can cause embolism?

A

Thrombosis:
- Inappropriate Clotting

Embolism:
- Migration of Clots

Emboli can be: Coagulated Blood, Amniotic Fluid, Gas, ect.

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6
Q

Hyperemia vs. Congestion

  • how does the presentation differ?
  • Passive or Active?
A

Hyperemia:

  • ACTIVE - MORE INFLOW
  • Active arteriolar dilation and Increased Blood flow
  • Results in flushing of the Skin (e.g. skin after exercise)

Congestion:

  • PASSIVE - LESS OUTFLOW
  • impaired outflow of venous blood from a tissue
  • Results in Cyanosis (from deoxyhemoglobin)
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7
Q

What are 4 results of chronic congestion?

A
  1. Cell death and Fibrosis
  2. Elevated Intravascular Pressures
  3. Edema
  4. Ruptured Capillaries Producing Focal Hemorrhages
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8
Q

What condition leads to nutmeg liver?

- features?

A

Chronic Passive Congestion of the Liver

  • Red, Depressed central Vein area (in lobule center)
  • Outter areas look brown and (liver colored)

***This happens when the liver is poorly perfused like in heart failure

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9
Q

In a histological section how would you differentiate between acute and chronic pulmonary congestion?

A

Acute:

  • Thickened Alveolar Walls (necrotic processes)
  • Transudate in Alveolar Lumen
  • Dilated Capillaries in Alveolar Wall

Chronic:

  • Fibrosis in Alveolar Walls (apoptotic processes)
  • HEMOSIDERIN laden macrophages from eating…
  • Blood from the alveolar lumen
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10
Q

What are 2 common causes of acute pulmonary congestion?

A
  1. Pulmonary Embolism

2. Myocardial Infarction

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11
Q

What are the terms for Edema in:

  • Thorax
  • Pericardium
  • Peritoneum
  • Internal and External Organs
A

Thorax:
- Hydrothorax

Pericardium:
- Hydropericardium

Peritoneum:

  • Ascites
  • Hydroperitoneum

Internal and External Organs:
- Anasarca

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12
Q

What does edema usually consist of?

A

Transudate

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13
Q

In what 3 ways does propping your legs up help you to reduce swelling in your legs?

A
  1. Decreases Hydrostatic Pressure on Capillaries
  2. Increases Venous Return
  3. ?????????
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14
Q

You see a patient with one leg significantly larger than the other, and it displays erythema, and calor. What should be your first thought?

A
  • You should think DVT (deep venous thrombosis)
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15
Q

Why is albumin important?

  • abundance?
  • what conditions result in albumin loss?
A
  • Major osmoregulatory Protein (maintains oncotic pressure)
  • Makes up 1/2 of all plasma Protein
  • Loss can lead to reduced Plasma Oncotic Pressure
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16
Q

When do you commonly see peau d’orange?

A

Failure Breast Lymphatics to Drain because they are obstructed (by cancer etc.)

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17
Q

What causes Filariasis and Elephantiasis?

A

Blood Parasite

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18
Q

What are some prerenal causes of renal failure?

A
  • Heart Failure
  • Shock (sudden and severe drop in blood pressure)
  • Other interuptions of bloodflow to the kidneys from sever injury or illness
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19
Q

What are some Intrarenal causes of Renal failure?

A

Direct Kidney damage via:

  • Inflammation
  • Toxins
  • Drugs
  • Infection
  • Reduced Blood Supply
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20
Q

What are some Postrenal causes of Renal failure?

A 
URINARY TRACT OBSTRUCTION
from:
- enlarged prostate
- kidney stones
- bladder tumor 
- injury
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21
Q

Poststreptococcal Glomerulonephritis and Acute renal failure have what physiologic effects in common?

A

They lead to excessive retention of Salt and Water

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22
Q

What is cardiac tamponade?

A
  • So much fluid gets into the pericardial sac that the heart can’t beat anymore (e.g. from Hemopericardium)
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23
Q

What is a hematoma?

A

Hemorrhage that has accumulated in tissue.

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24
Q

What are petechiae?

- when are they often seen?

A

1 to 2 mm hemorrhages into the skin or mucosal surfaces

  • Platelet Defects
  • Vit C deficiency
  • Asphyxiation
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25
Q

What are Purpura?

- when are they often seen?

A

3-5 mm hemorrhages into the skin (or mucosal surfaces)

  • Trauma
  • Vascularitis
  • Increased Vascular Fragility (old ppl.)
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26
Q

what are Ecchymoses?

A

Bruises

- 1 to 2 cm subcutaneous hematomas

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27
Q

What can be found in dense bodies?

- aka ∂ granules

A
  • ADP and ATP
  • Ca2+
  • Histamine
  • Seratonine
  • Epinephrine
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28
Q

What 4 general steps make up Hemostasis and Thrombosis?

A
  1. Vasocontriction
  2. Primary Hemostasis
  3. Secondary Hemostasis
  4. Antithrombotic Counterregulation
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29
Q

What Causes the Vasocontriction phase of Hemostasis and Thrombosis?

A
  • Endothelin released from the Damaged Epithelium

* Reflex Vasoconstriction

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30
Q

What are the 5 steps of Primary Hemostasis and what factors are involved?
- what does this process ultimately form?

A
  1. Type IV collagen is exposed and Platelets bind to it as well as to vWF
    - Platelet binding to vWF is mediated by Gp1b
  2. Platelet changes shape to become flattened
  3. Platelets release granule contents (ADP most imp) and TXA2
  4. ADP causes Gp2a/3b upregulation and TXA2 recruits more platelets that stick together
  5. Platelets aggregate and Primary plug is formed
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31
Q

What are the Steps of Secondary Hemostasis?

A
  1. Tissue factor gets released from the cells, coagulation cascade is not triggered (also XII is triggered by exposure of type IV collagen)
  2. Thrombin is generated
  3. Fibrin is Polymerized on the Platelets with GpIIb/IIIa binding fibrin and creating bridges between platelets
  4. Secondary STRONG hemostatic plug is formed
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32
Q

What factors are involved in antithrombic counterregulation?

A

Endothelial cells expresses factors that help breakdown the fibrin:

  • t-PA
  • Thrombomodulin
  • Adenosine Diphosphatase
33
Q

What factors specifically are responsible for:

  1. Platelet Adhesion
  2. Platelet Activation
  3. Aggregation
A
  1. GpIb to vWF
  2. conformational change that allows…
  3. Aggregation of GpIIb/IIIa binding to fibrinogen
34
Q

What diseases result from lack of:

  • vWF
  • GpIb
  • GpIIb/IIIa
A 
vWF = von Willebrand Disease
GpIb = Bernard-Soulier Syndrome
GpIIb/IIIa = Glanzmann Thrombasthenia
35
Q

What does Factor XIIIa do?

A

Cross-links Fibrin Polymers

36
Q

What 3 factors always play into thrombosis?

A
  1. Endothelial Injury
  2. Abnormal Blood Flow
  3. Hypercoagulability
37
Q

What are some factors that might cause endothelial injury leading to thrombosis?

A
  • Hypertension
  • Hypercholesterolemia
  • Bacterial Products
  • Radiation injury
  • cigarettes
  • homocysteinemia
38
Q

What are some factors that might cause abnormal blood flow that would lead to thrombosis?

A
  • Stasis = venous thrombi
  • Aortic and Arterial Dilations
  • Dilated artria
39
Q

What are some factors that can cause hypercoagulability?

A
  • Deficiency of Protein C or S
  • Cancer
  • Late Pregnancy (post pardum)
  • Birth control
  • Immobility
40
Q

Where is a saddle embolus seen?

A

In the main pulmonary arteries

41
Q

How do you figure out if a clot happened while someone was alive or if it happened after they were dead?

A
  1. LOOK FOR LINES OF ZAHN (layered lines of light and dark created from fibrin)
  2. Usually is loosely associated with the blood vessel
42
Q

What kind of thrombi occur in the heart chambers or in the aortic lumen?

A

Mural Thrombi

43
Q

What are the 4 possible fates of a thrombi?

A

Propagation - thrombus builds up and gets bigger
Embolization - becomes mobile
Dissolution - if they don’t embolize they’ll get broken down
Organization and recanalization - they can become calcified and form new canals through the tissue allowing small amounts of blood to pass

44
Q

What is the Primary consequence of Systemic Embolization?

A

Ischemic Necrosis = Infarction

45
Q

If a thrombus forms slowly over time and completely occludes a vessel, how can the person be asymptomatic?

A
  • Collateral Blood supply can be created if the thrombus forms slowly enough
46
Q

What are 5 places where Red Infarcts are commonly seen?

A
  • Testicles
  • Lungs
  • Brain
  • G.I. Tract
  • Liver
47
Q

**Why do we get a red infarct vs. a white infarct?

A

Red:

  • VENOUS insufficiency (testicle)
  • Tissue get Reperfused (brain)
  • Dual blood supply (liver, Lungs, G.I.)

White:

  • ARTERIAL insufficiency
  • Not Reperfused
  • Single blood supply
48
Q

What factors determine whether an occlusion results in an infarction?

A
  1. Collateral Blood Supplies
  2. Rate at which obstruction Develops
  3. Intrinsic Susceptibility to Ischemic Injury
  4. Blood Oxygenation
49
Q

What are the general results of shock?

A

Impaired Tissue Perfusion and Cellular Hypoxia

50
Q

What are the 3 most common types of shock?

- and their causes

A
  • Cardiogenic Shock - low cardiac output due to myocardial pump failure
  • Hypovolemic shock - low cardiac output due to loss of blood or plasma volume
  • Septic shock - arterial vasodilation and venous blood pooling that stems from systemic immune response to microbial infection
51
Q

What are the 3 stages of shock?

A
  1. NONPROGRESSIVE STAGE - reflex compensatory mechanisms are activated and vital organ perfusion is maintained
  2. PROGRESSIVE stages - tissue HYPOperfusion and onset of worsening circulatory and metabolic derangement, including Acidosis
  3. IRREVERSIBLE stage - cellular tissue and injury is so severe that even if hemodynamic defects are corrected, survival is unlikely
52
Q

What are some signs of severe Sepsis?

A
  • Significantly Decreased Urine Output
  • Abrupt change in Mental Status
  • DECREASED PLATELET count
  • Difficulty Breathing
  • Abnormal Heart Pumping Function
  • Abdominal pain
53
Q

What causes decreased platelet count in septic shock?

A

DIC

54
Q

T or F: if someone has 2 of the 3 following signs then they are probably septic

  • Fever
  • Tachycardia
  • Tacypnea
A

TRUE

55
Q

What causes elephantiasis?

A

Lymphatic Obstruction

56
Q

T or F: the cause of edema with congestive heart failure is always increased hydrostatic pressure

A

True

57
Q

What is a good indicator of edema in squamous cells?

A
  • When you can see the outline of each cell because there are spaces between cells then there is squamous cell edema
58
Q

You cut open the lungs of a patient that died of heart failure. What do you expect to see?

A
  • Bronchus filled with frothy proteinaceous edema fluid from the alveoli
59
Q

What is usually the 1st place you see edema in people with nephrotic syndrome?

A

Periorbital edema under their eyes

60
Q

What causes depenedent pitting edema?

A

High Hydrostatic pressure at great distances from the heart (in the feet)

61
Q

Why do Ecchymosis convert from Red-blue to Blue-Green to Gold-Brown?

A

These color changes are the result of hemoglobin breakdown

62
Q

When are you most likely to see a Fat Thrombosis?

A

Fractures of the Long Bones

63
Q

Why do Thombi inevitably form around vascular Catheters?

A
  • Endothelial Injury
  • Impeded Blood Flow (stasis)
  • Thrombogenicity or Foreign material
  • Turbulent Blood Flow
64
Q

What are 6 genetic causes of Hypercoagulability?

A
  1. Factor V Leiden Mutation *KNOW THIS
  2. Prothrombin G20210A mutation
  3. Methylenetetrahydrofolate reductase homozygous C677T mutation
  4. Anti-thrombin-3 deficiency
  5. Protein C deficiency
  6. Protein S deficiency
65
Q

How do Pulmonary Infarct kill lung tissue if there is a dual blood supply? and why do they turn Red?

A

85% of bs is from pulmonary arteries - these are the ones that get clogged because they are in venous circulation

15% is from bronchial arteries - this typically not enough to keep the tissue alive, but is enough to pump it full of blood

66
Q

What tissue injury response leads to the bleeding stopping in seconds?

A

Vasocontriction

note: clotting takes minutes

67
Q

What is a thrombotic mass on a heart valve called?

- where does it go if it dislodges?

A

Vegetation

Right Valve (Tricuspid) 
- Emboli would go to the LUNGS 
Left Valve (Bicuspid) 
- Emboli would go the BRAIN, SPLEEN, or KIDNEY
68
Q

What should a False positive on a syphilis test alert you to?

A

SLE - however, more than just SLE patients have this so more Dx tests would need to be done

69
Q

Why do SLE patients have False Positives on Syphilis tests?

- what are the risks associated with this process?

A
  • Anti-Cardiolipin Abs are present in the blood of some SLE patients and Cardiolipin agglutination is what is used to test for syphillis

RISKS:
- THROMBOSIS - especially during pregnancy (can cause miscarriages)

70
Q

If you want to bust a clot up, why would you give t-PA over heparin?

A

t-PA is given to Bust up Clots because it ACTIVATES PLASMINOGEN to cleave FIBRIN

Heparin just activates Anti-thrombin III and therefore just SLOWS down the clotting process

71
Q

When is it common to see Acute Pulmonary Congestion?

A
  • After an MI
72
Q

What is the most common inherited mutation causing a predisposure to blood clots?

A

Factor V Mutation that prevents Protein C regulation

73
Q

T or F: TXA2 is present in delta granules of platelets.

A

FALSE

74
Q

How does protein C get converted to its active form?

A
  • Thrombomodulin binds Thrombin

- Thrombin is then able to Activate Protein C

75
Q

T or F: arterial clots can make it into venous circulation.

A

False, the clot couldn’t cross through capillary beds

76
Q

T or F: infarction of the liver is rare

A

True, this is because it has a duel blood supply

77
Q

What mediator is responsible for preventing downstream clotting?

A

PGD2 (prostacyclin)

78
Q

Why do alcoholic have trouble with bleeding?

A

Factors II, VII, IX, and X are all made in the liver

CMOD-Block 2 Path (22 decks)

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