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(OMS1) MOD Exam 1 > Lecture 4: Hemodynamics and Shock > Flashcards

Lecture 4: Hemodynamics and Shock Flashcards

1
Q

What is edema?

A

Fluid collection in the interstitial space

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2
Q

What is an effusion?

Can you state an example of a space where an effusion would exhist in?

A

Fluid collection in a potential space (body cavity)

  • Pleural space
  • Peritoneal space (ascites)
  • Pericardial space
  • Joint space
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3
Q

What are the two ways you can get an increased intravascular hydrostatic pressure?

A
  • Sodium and water retention
  • Congestion
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4
Q

What is hyperemia?

A

Too much blood is arriving

(physiologic, occurs after a workout for example)

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5
Q

What is congestion?

A

Not enough blood is leaving

(pathologic)

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6
Q

What controls hyperemia and how does it cause congestion?

A

Precapillary sphincter regulates how much blood can pass through the capillary bed

Congestion happens when there is too much blood stuck in the venous side and cannot leave, backflow through the precapillary sphincter

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7
Q

Soft tissue edema/pitting edema is usually indicative of what?

A

Heart failure

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8
Q

Describe the mechanism of heart failure leading to edema/effusion

A

During heart failure, the heart fails to perfuse the body.

THEN

When the kidneys are underperfused, the kidneys will activate the RAAS system in order to retain water

This leads to the overall increase in dilute water retention –> hypervolemia —> edema/effusion secondary to increased hydrostatic pressure

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9
Q

What other presentations are associated with heart failure?

A

Pulmonary edema (from left ventricular failure causing blood to backflow to the lung)

Pleural effusions

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10
Q

What are the effects of liver failure?

A

Edema

Ascites

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11
Q

Part 1

Why do patients with liver failure get edema?

(specific to a particular protein mechanism)

A

With liver failure, the liver fails to produce normal byproducts.

Liver is responsible for producing ALBUMIN

If liver is nonfunctional, there is LESS albumin > decreased colloid osmotic pressure int he vessel > fluid leaks out

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12
Q

How else does liver failure cause edema?

A

usually secondary to CHF, increased intravascular hydrostatic pressure > Portal hypertension > congested passage through the liver > distension of hepatic portal system > fluid leaks out to the peritoneal space > ascites

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13
Q

What are the two ways renal disease can cause edema?

A

-Retained sodium and water (leads to increased intravascular hydrostatic pressure) = pitting edema

-Nephrotic syndrome (excess protein loss in urine leads to decreased oncotic pressure) = pitting edema

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14
Q

Can you guess what is happening here?

A

Protein deficiency (Kwashiorkor)

Insufficient albumin (reduced plasma oncotic pressure)

Not enough protein ingested : malnutrition

Not enough protein produced : liver failure

Too much protein lost: kidney disease with nephrotic syndrome

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15
Q

This is image represents what type of edema?

A

Lymphatic obstruction, usually localized to area of obstruction/trauma or inflammation

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16
Q

Can you give a few examples of what would cause localized lymphedema?

A

Infection

Inflammation

Trauma

Tumors

Surgery

Malformations

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17
Q

You have identified your patient is releasing exudate. What is most likely causing this protein rich fluid to escape?

A

Sepsis

Inflammation

Burns

*All three of these lead to increased vascular permeability

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18
Q

What is this histologic slide showing?

A

Pulmonary edema

*Notice how SOME of the alevolar spaces are filled with air, and others have a pink tinge to them. ALL of the alveolar spaces SHOULD be filled with air. The pink spaces are abnormal fluid accumulation

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19
Q

What are these slides revealing?

Name the cells!

A

CHRONIC Pulmonary edema

*hallmark: chronic congestions shows an increase in hemosiderin-laden macrophages “heart failure cells”

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20
Q

Hepatic congestion is due to the obstruction/flow reduction of the ______________

A

Central vein

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21
Q

What is this gross specimen revealing?

What causes this to happen?

A

“Nutmeg liver”

often due to CHF, central vein is congested, so deoxygenated blood flowing through the liver back to the IVC back flows to the lobules and causes centrilobular necrosis = nutmeg liver

Dark areas=dying hepatocytes

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22
Q

What is the initial step in hemostasis?

A

Reflexive vasoconstriction

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23
Q

Why is neurogenic reflexive vasoconstriction an effective first step in hemostasis?

A
  • Reduces blood flow to the area so you don’t bleed as much!
  • Reduces the surface area of the affected area to allow hemostasis to occur
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24
Q

What is the “goal” of primary hemostasis?

A

Formation of a Platelet Plug

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25
**Weibel palade bodies** are useful indicators of what cells? They are a significant source of?
Endothelial cells vWF
26
What happens if you have a deficiency in vWF?
Von Willebrand Disease Inability of platelets to stick down, Platelet **adhesion** will not occur
27
What happens if there is a deficiency in **Gp1b** receptor?
**Bernard Soulier Syndrome** Platelet adherance disorder
28
How can you morphologically identify the difference between _Von Willebrand disease_ and _Bernard Soulier syndrome?_
Bernard Soulier syndrome will have morphological defects in the **platlets** themselves! That's because receptor **Gp1b** is ON THE PLATELETS \*ON THE RIGHT=Bernard Soulier syndrome platelets, HUGEEEE platelets
29
What occurs during **platelet activation?**
After adhesion... Conformational change (-) Negatively charged surface _GpIIb-IIIa_ change and create _fibrinogen links_ Secretion initiated by thrombin, release of **ADP** and **Thromboxane A2**
30
What does **aspirin** inhibit? Why does that make sense?
Thromboxane A2 Blocking platlet aggregation
31
What occurs during the third step in primary hemostasis?
Aggregation
32
Describe what happens during **aggregation** in primary hemostasis?
Conformational change in the **GpIIb-IIIa complex** in activated platelets allow for **bivalent binding** of fibrinogen and subsequent cross-linking
33
What is the name of the disease associated with a deficiency of **GpIIb-IIIa**?
Glanzmann Thrombasthenia
34
How do we know if something is wrong with primary hemostasis? What are the clinical questions we can ask?
skin and mucosal bleeding Questions: Nose bleeds? Oral bleeding with teeth brushing? Easy bruising? Heavy menstrual cycle?
35
What are the laboratory methods to determine there is something wrong with primary hemostasis?
Bleeding time (outdated) Platelet function studies (outdated) PFA 100 (modern) Flow cytometry (modern)
36
**Thrombocytopenia** Mechanism? Platlet count? Platelet adhesion? Platelet aggregation?
Mechanism = loss or impaired production of platlets Platlet count= LOW Platelet adhesion= YES Platelet aggregation= YES
37
**Von WIllebrand disease** Mechanism? Platlet count? Platelet adhesion? Platelet aggregation?
Mechanism= Inherited **lack of vWF** Platlet count= Normal Platelet adhesion= NO Platelet aggregation= YES
38
**Bernard-Soulier disease** Mechanism? Platelet count? Platelet adhesion? Platelet aggregation?
Mechanism= Abnormal **GpIb** Platelet count= Normal Platelet adhesion= NO Platelet aggregation= YES
39
**Glanzmann's Thrombasthenia** Mechanism? Platelet count? Platelet adhesion? Platelet aggregation?
Mechanism= Abnormal **GpIIb-IIIa** Platelet count= Normal Platelet adhesion= YES Platelet aggregation=NO
40
Generally, what are the three steps of primary hemostasis?
Adhesion Activation/secretion Aggregation
41
What is the goal of **secondary hemostasis?**
Forming a **fibrin clot**
42
Draw the coagulation cascade with the **intrinsic** and **extrinsic pathway**
43
What does aPTT measure? WHat does PT measure?
aPTT = intrinsic pathway clotting time PT = extrinsic pathway clotting time
44
Aliases for clotting cascade: What is the name of **Factor I? Ia?**
I =Fibrinogen, Ia=Fibrin \*activated form is **(a)**
45
Aliases for clotting cascade: What is the name of Factor II? IIa?
II= Prothrombin, IIa=Thrombin
46
Aliases for clotting cascade: What is the name of Factor VIII?
Antihemophilic A Factor (AHF)
47
What are the **vitamin k-dependent factors?**
II VII IX X
48
How does **coumadin** work?
Blocks the formation of active **V****itamin K** By doing this, you knock out factors **II, VII, IX, X** THEN you don't clot as much!
49
What are the three major functions of **Thrombin?**
- Stabilizes fibrin - Activates platelets - Activates receptors on inflammatory cells and endothelium
50
What are the dermatologic manifestations of a **defect in hemostasis?**
(A) Petechiae (small) (B) Purpura (larger) (C) Ecchymosis (palpable)
51
What is a disease that is commonly associated with **factor deficiencies?**
Hemarthrosis Bleeding into a joint space
52
What is the last step in secondary hemostasis?
STOPPING IT! Fibrinolysis and limitation of clot formation - Arrest in clot formation - Resorption of clot - Tissue repair
53
What can terminate coagulation?
1. Blood flow by washing away clotting factors (not scaffold for platelet aggregation) 2. Plasmin 3. Endothelium releasing anti-thrombolytic factors
54
What is the body's endogenous clot dissolver?
Plasmin
55
What activates **plasmin?**
t-PA
56
How does the endothelium have antithrombotic effects?
Staying intact (not exposing the tissue factor) Release heparin like molecules (Adenosine diphosphatase, prostacyclin, NO) that inhibit platelets Release thrombomodulin which couples with thrombin \> activates protein C \> lyses Factors Va and VIIIa
57
What are ALL the **vitamin-k dependent factors?**
II VII IX X Protein C Protein S
58
# Define a: Thrombus Embolus
Thrombus: Occlusion Embolus: Traveling occlusion
59
What is **Virchow's tirad?**
Risk factors associated with **Thrombosis**
60
Virchow's triad part 1: Describe what happens when you damage the endothelium?
decrease of NO and activation of adhesion molecules \> Endothelium becomes **PROTHROMBOTIC** because it got damaged (decreased thrombomodulin and activation of tPA inhibitors)
61
Virchow's triad part 2: What happens with alterations in blood flow?
transition from laminar to turbulent flow leads to endothelial damage
62
Virchow's tirad part 2: What are some causes blood flow turbulence?
Internal obstructions (atherosclerosis), compressions (non-contractile myocardium), inadequate heart chamber function (Afib/stasis), aneurysm, hemorrhoids can all contribute to formation of thrombus
63
Virchow's triad part 3: Hypercoagulability What are the **primary genetic causes?**
Deficiency of antithrombotic factors: - Antithrombin (III) deficiency) - Protein C deficiency - Protein S deficiency Increased prothrombotic factors: - Factor Va - Prothrombin
64
What are the **secondary (acquired) causes** of hypercoagulability?
Prolonged bed rest/immobilization MI Cancer A fib
65
What are the ways a DVT can present?
66
What are you most concerned about a DVT embolus dislodging?
Pulmonary embolism
67
Clinical presentations of PE?
Large ones can be instantaneously fatal Small emboli can lodge into smaller vessels and can present with dyspnea, or be small enough to be asymptomatic
68
What is the mechanism of action of **factor V leiden mutation?**
Mutation in factor V that makes it **resistant to cleavage by protein C** Therefore....cannot turn off coagulation
69
How can you test for **Factor V Leiden mutation?**
Direct genetic testing or APC resistance testing
70
When to suspect primary hypercoagulable states? What should you consider as differentials for these patients?
An initial event occured: DVT, PE No provoking factors Young age \<40 Strong family history Genetic causes of thrombosis: Factor V Leiden, ATIII def, protein C and S def, Prothrombin G20210A mutation
71
What is **Heparin-induced thrombocytopenia?**
**Prothrombotic but thrombocytopenic state** caused by antibodies to PF4-heparin-platelet complex sheared platelets causes thrombocytopenia, but these platelets can also activate other platelets, leading to prothrombotic state, often leads to necrosis
72
What is **Antiphospholipid antibody syndrome?** **What are the symptoms of Antiphospholipid antibody syndrome?**
Aquired Hypercoaguable state where **Antibodies** against plasma proteins that bind to **phospholipids** -arterial or venous thrombosis, unexplained miscarriage/stillbirth
73
What are **lines of zahn?**
Pathologic finding that indicates a thrombus/embolus occurred during **active blood flow** (during the patient's life)
74
What are the fates of thrombi?
Propagation Embolization Dissolution (if treated with tPA within 6 hours of onset) Organization (where CT form aggregates around thrombus) Recanalization
75
What are the 5 types of emboli we discussed in lecture?
- Thromboemboli (blood clot) - Fat/marrow emboli - Air emboli - Septic emboli - Amniotic fluid emboli
76
Fat Emboli What are some clinical symptoms?
Caused by a fracture or soft tissue trauma **BONE MARROW/(fat)** is introduced into circulation respiratory distress, mental changes, frequently seen as a post mortem finding due to resuscitation prior to demise
77
What are common causes of **Air embolism?**
Cardiac catheterization Deep sea diving! The Bends, "Caisson disease" (N2 stuck in periphery and forms bubbles causing bends)
78
What is an **Amniotic fluid embolism?**
More of a **severe anaphylactic** response to amniotic fluid Sudden dyspnea, cyanosis, shock, subsequent pulmonary edema
79
What can cause septic emboli?
Endocarditis where Heart valve has become infected and Infective vegetations break off and manifest in other sites
80
What are the peripheral manifestations of **septic emboli secondary to endocarditis**
Skin microemboli: Janeway lesions (purpuric) Retinal microemboli : Roth spots Vascular damage in nail bed: Splinter hemorrhage
81
What is a **white thrombus**?
ARTERIAL Platelet rich Occur in high shear stress ARTHEROSCLEROSIS Coronary, cerebral arteries, bowel results in **Infarction**
82
What is a **red thrombus?**
**Venous** Red cell rich Occurs during STASIS Lower extremities
83
What are disease that occur when **white thrombi** collect?
Strokes Heart attacks
84
What is the difference of red vs white infarct?
Red: happens in tissues supplied by more than 1 vessel (lungs) White: happens in tissues supplied by a single vessel (spleen)
85
What is collateral circulatino? How does it happen?
Protective mechanism from infarction where new vessels forming downstream an obstruction, happens if occlusion occurs slowly
86
What are the mechanisms of shock?
Shock is inadequate tissue oxygenation to meet physiological needs Mechanisms: Cardiogenic (heart can't pump well) Hypovolemic: blood flow is non ideal Inflammatory: overactive immune respone causing the body to require more oxygenation than normal Neurogenic: autonomic disruption leading to vasodilation and decreased vascular resistance Anaphylactic: IgE mediated leading to decreased vascular resistance
87
How does septic shock happen?
1. Inflammation 2. endothelium cell activation increases permiability and vasodilation = hypovolemia and hypotension 3. endothelial cell dysfunction = becomes procoaguant and forms thrombus
88
What is the final consequence of shock? What are the classical systemic symptoms of shock?
decreased tissue oxygenation = hypoxic tissue injury heart failure, hypotension, renal failure, lung failure, coma

(OMS1) MOD Exam 1 (5 decks)

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