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MOD Exam 1 (Lecture material) > Lecture 3: Hemodynamics and Shock I (Dr. Singh) > Flashcards

Lecture 3: Hemodynamics and Shock I (Dr. Singh) Flashcards

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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?

A

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 –> edema/effusion

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9
Q

What else is associated with heart failure?

A

Pulmonary edema

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

WIth LESS albumin, means more leaky fluid!

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12
Q

Part 2

Why do patients with liver failure get edema?

Second mechanism

A

Portal hypertension

leads to ascites

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13
Q

What are the two methods of getting edema through liver failure?

A
  • Decreased production of albumin
  • Portal hypertension
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14
Q

What are the two ways renal disease can cause edema?

A

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

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

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15
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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16
Q

This is image represents what type of edema?

A

Lymphatic obstruction

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17
Q

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

A

Infection

Inflammation

Trauma

Tumors

Surgery

Malformations

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18
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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19
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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20
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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21
Q

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

A

Central vein

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22
Q

What is this gross specimen revealing?

A

“Nutmeg liver”

Shows the pathology of chronic hepatic congestion

Dark areas=dying hepatocytes

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23
Q

What is the initial step in hemostasis?

A

Reflexive vasoconstriction

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24
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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25
What is the "goal" of **primary hemostasis?**
Formation of a **Platelet Plug**
26
**Weibel palade bodies** are useful indicators of what cells? They are a significant source of?
Endothelial cells vWF
27
What happens if you have a deficiency in vWF?
Von Willebrand Disease Inability of platelets to stick down, Platelet **adhesion** will not occur
28
What happens if there is a deficiency in **Gp1b** receptor?
**Bernard Soulier Syndrome** Platelet adherance disorder
29
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
30
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**
31
What does **aspirin** inhibit? Why does that make sense?
Thromboxane A2 Blocking platlet aggregation
32
What occurs during the third step in primary hemostasis?
Aggregation
33
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
34
What is the name of the disease associated with a deficiency of **GpIIb-IIIa**?
Glanzmann Thrombasthenia
35
How do we know if something is wrong with primary hemostasis? What are the clinical questions we can ask?
Nose bleeds? Oral bleeding with teeth brushing? Easy bruising? Heavy menstrual cycle?
36
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)
37
**Thrombocytopenia** Mechanism? Platlet count? Platelet adhesion? Platelet aggregation?
Mechanism = loss or impaired production of platlets Platlet count= LOW Platelet adhesion= YES Platelet aggregation= YES
38
**Von WIllebrand disease** Mechanism? Platlet count? Platelet adhesion? Platelet aggregation?
Mechanism= Inherited **lack of vWF** Platlet count= Normal Platelet adhesion= NO Platelet aggregation= YES
39
**Bernard-Soulier disease** Mechanism? Platelet count? Platelet adhesion? Platelet aggregation?
Mechanism= Abnormal **GpIb** Platelet count= Normal Platelet adhesion= NO Platelet aggregation= YES
40
**Glanzmann's Thrombasthenia** Mechanism? Platelet count? Platelet adhesion? Platelet aggregation?
Mechanism= Abnormal **GpIIb-IIIa** Platelet count= Normal Platelet adhesion= YES Platelet aggregation=NO
41
Generally, what are the three steps of primary hemostasis?
Adhesion Activation/secretion Aggregation
42
What is the goal of **secondary hemostasis?**
Forming a **fibrin clot**
43
Draw the coagulation cascade with the **intrinsic** and **extrinsic pathway**
44
What does aPTT measure? WHat does PT measure?
aPTT = intrinsic pathway clotting time PT = extrinsic pathway clotting time
45
Aliases for clotting cascade: What is the name of **Factor I? Ia?**
I =Fibrinogen, Ia=Fibrin \*activated form is **(a)**
46
Aliases for clotting cascade: What is the name of Factor II? IIa?
II= Prothrombin, IIa=Thrombin
47
Aliases for clotting cascade: What is the name of Factor VIII?
Antihemophilic A Factor (AHF)
48
What are the **vitamin k-dependent factors?**
II VII IX X
49
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!
50
What are the three major functions of **Thrombin?**
- Stabilizes fibrin - Activates platelets - Activates receptors on inflammatory cells and endothelium
51
What are the dermatologic manifestations of a **defect in hemostasis?**
(A) Petechiae (small) (B) Purpura (larger) (C) Ecchymosis (palpable)
52
What is a disease that is commonly associated with **factor deficiencies?**
Hemarthrosis Bleeding into a joint space
53
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
54
What is the body's endogenous clot dissolver?
Plasmin
55
What activates **plasmin?**
t-PA
56
What are three **endothelium factors** that **inhibit platelets?**
Adenosine diphosphatase Prostacyclin Nitric oxide
57
What mechanism in the endothelium turns off coagulation?
When **Thrombin** sees a normal and healthy endothelial cell, it binds to the receptor **thrombomodulin**. This creates **activated protein C** which TURNS OFF COAGULATION
58
What are ALL the **vitamin-k dependent factors?**
II VII IX X Protein C Protein S
59
# Define a: Thrombus Embolus
Thrombus: Occlusion Embolus: Traveling occlusion
60
What is **Virchow's tirad?**
Risk factors associated with **Thrombosis**
61
Virchow's triad part 1: Describe what happens when you damage the endothelium?
Endothelium becomes **PROTHROMBOTIC**
62
Virchow's triad part 2: What happens with alterations in blood flow?
Turbulent blood flow is BAD Can feed into endothelial injury as well!!!
63
Virchow's tirad part 2: What happens with alterations in blood flow?
Internal obstructions, compressions, inadequate heart chamber function, aneurysm, hemorrhoids can all contribute to _formation of a thrombus_
64
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
65
What are the **secondary (acquired) causes** of hypercoagulability?
Prolonged bed rest/immobilization MI Cancer A fib
66
What are the ways a DVT can present?
67
What are you most concerned about a DVT embolus dislodging?
Pulmonary embolism
68
Read pages 123-125 of robbins per Dr. Singh
Genetic: Factor V Leiden mutation Aquired: Heparin-induced thrombocytopenia Antiphospholipid antibody syndrome
69
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
70
How can you test for **Factor V Leiden mutation?**
Direct genetic testing or APC resistance testing
71
How to suspect primary hypercoagulable states?
An initial event occured: DVT, PE No provoking factors Young age \<40 Strong family history
72
What is **Heparin-induced thrombocytopenia?**
AQUIRED Hypercoagulable state **Prothrombotic state** caused by antibodies to PF4-heparin
73
What is **Antiphospholipid antibody syndrome?**
Aquired Hypercoaguable state **Antibodies** against plasma proteins that bind to **phospholipids**
74
What are **lines of zahn?**
Pathologic finding that indicates a thrombus/embolus occurred during **active blood flow** (during the patient's life)
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
Describe a : Fat Emboli
Caused by a fracture or soft tissue trauma **BONE MARROW/(fat)** is introduced into circulation \*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"
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 is **endocarditis?**
Heart valve has become infected Infective vegetations break off and manifest in other sites
80
What are the peripheral manifestations of **endocarditis?**
Skin microemboli: Janeway lesions (purpuric) Retinal microemboli : Roth spots Vascular damage in nail bed: Splinter hemorrhage
81
Read infarct section Robbins pages 129-130
82
What is a **white thrombus**?
ARTERIAL Platelet rich Occur in high shear stress ARTHEROSCLEROSIS Coronary, cerebral arteries
83
What is a **red thrombus?**
**Venous** Red cell rich Occurs during STASIS Lower extremities
84
What are disease that occur when **white thrombi** collect?
Strokes Heart attacks
85
What is the definition of **shock?**
Tissue oxygen and nutrient delivery is inadequate to meet physiologic needs
86

MOD Exam 1 (Lecture material) (5 decks)

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