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Pathobiology > Circulatory Disturbances > Flashcards

Circulatory Disturbances Flashcards

1
Q

The relative proportion of intracellular to extracellular body fluid, and what are the extracellular fluid spaces? Make a distinction between extravascular and intravascular

A

2/3 intracellular
1/3 extracellular

Major of extracellular fluid is interstitial fluid (extravascular)

Intravascular spaces (plasma) make up a smaller component

Smallest component is third space fluid in body cavities (also extravascular)

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2
Q

Where in the capillary is water driven out of the plasma and reabsorbed?

A

Driven out at arterial end by hydrostatic pressure

Uptaken at venous end by colloid osmotic (oncotic) pressure via plasma proteins

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3
Q

How does capillary permeability affect oncotic pressure?

A

If permeability is too high, there is a loss of oncotic pressure because plasma proteins will seem into the extravascular interstitium, so there will be no forces to reuptake water (as in exudative edema in acute inflammation)

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4
Q

Define: edema vs anasarca vs hydrothorax vs ascites.

A

Edema - increased interstitial fluid
Anasarca - Widespread, severe systemic edema
Hydrothorax - edema in thoracic cavity
Ascites - edema fluid in peritoneal cavity

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5
Q

What are the protein, cellular, and specific gravity characteristics of transudative edema?

A

Protein - low (not exudative)
Specific gravity - low (few proteins)
Cells - few

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6
Q

What is the definition of transudative edema and what are its two umbrella causes?

A

Edema due to NORMAL vascular capillary permeability

  1. Increased intravascular hydrostatic pressure
  2. Decreased plasma oncotic pressure
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7
Q

What things can cause increased intravascular hydrostatic pressure?

A
  1. Venous obstruction
  2. Heart failure -> leads to congestion and fluid buildup
    Left side -> pulmonary edema
    Right side -> generalized systemic edema
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8
Q

What two things can lead to decreased plasma oncotic pressure?

A
  1. Decreased protein synthesis -> liver disease or kwashiorkor
  2. Increased protein loss -> nephrotic syndrome
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9
Q

What is a frequent exacerbating complication of edema?

A

Decreased plasma volume activates the RAA system, reabsorbing more sodium and water. If edema source is not corrected, this new extra water + sodium will accumulate further in interstitium.

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10
Q

What are the protein, cellular, and specific gravity characteristics of exudative edema?

A

Protein - high (exudative)
Specific gravity - high (many proteins)
Cells - many

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11
Q

What is the definition of exudative edema and give two causes?

A

Edema due to INCREASED vascular permeability

  1. Acute inflammation
  2. Angiogenesis of malignancies (new vessels are very leaky)
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12
Q

What is the final type of edema other than exudative and transudative and give two causes.

A

Edema due to lymphatic obstruction

  1. Infection blocking lymph drainage -> i.e. filariasis
  2. Maligancy physically blocking lymph drainage
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13
Q

What does severe edema of the subcutaneous soft tissue cause, and what is it depend on (in terms of where it’s located)?

A

Causes a pitting edema
-> dependent on gravity. If you are standing, edema will be in your legs. If you are lying down, edema may be in your pelvis

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14
Q

How does edema of the lungs appear grossly?

A

Heavy & wet lungs

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15
Q

What is the microscopic progression of lung edema and when does this lead to dyspnea? What does this lead to on radiograph?

A
  1. First spills out of capillaries into alveolar septae
    - > leads to Kerley B lines on X-ray
  2. Pneumocyte occluding junctions burst due to increased pressure -> fluid accumulates in alveolar airspace
    - > this leads to dyspnea and interstitial fluid on X-ray
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16
Q

Why is transudative edema in the lung very bad news?

A

It predisposes to infection

-> sitting fluid can house bacteria which will cause exudative edema later (pneumonia)

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17
Q

How does edema appear grossly in the brain, and what are the clinical consequences?

A

Gyri become flattened and compressed, with a heavy / swollen brain.

Complications:

  1. Herniation -> i.e. cerebellar tonsils through foramen magnum
  2. Vascular compression
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18
Q

What is the definition between congestion and hyperemia?

A

Congestion -> increased intravascular blood due to impaired outflow
- PASSIVE process, will result in more deoxygenated blood reaching capillary

Hyperemia -> increased intravascular blood due to expanded inflow
-ACTIVE process, will result in more oxygenated blood reaching capillary

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19
Q

How are you likely to tell the difference between hyperemia and congestion in the lung?

A

Both will have pulmonary capillaries filled up with RBCs

Congestion: More likely in the setting of transudative edema and few immune cells

Hyperemia: More likely in the setting of acute inflammation, as inflammatory cells are actively inducing the increased RBCs

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20
Q

How does chronic congestion of the lung appear different grossly than acute congestion?

A

Acute - lung will be heavy and wet, as edema

Chronic - lung will be heavy and dry, rusty brown due to iron accumulation from chronic RBCs

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21
Q

What cells are definitive for chronic congestion in the lungs?

A

Heart failure cells - hemosiderin-laden macrophages in the alveoli
-> eating up RBCs which sometimes leak out of capillaries from microhemorrhages due to congestion

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22
Q

What happens to the alveolar septae in chronic lung congestion?

A

Alveolar septal fibrosis

due to fibroblasts losing contact with ECM when they are exposed to so much edema chronically

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23
Q

What can cause congestion in the liver and what is its appearance grossly?

A
  1. Right-sided heart failure
  2. Obstruction of hepatic venous drainage

Grossly: “Nutmeg liver” -> looks like the inside of a nutmeg

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24
Q

What are the acute vs chronic effects of liver congestion? What areas of the liver are susceptible?

A

Acute: centrilobular sinusoids expand (central vein is the drain)

Chronic:
Centrilobular necrosis or atrophy, with accumulation of fibrosis and hemosiderin-laden macrophages
Periportal - normal or fatty change

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25
Q

Define hemorrhagic diathesis.

A

A predisposition to bleed

Diathesis = a disposition to suffering a particular medical condition

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26
Q

Define hematoma

A

Hemorrhage within a tissue

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27
Q

What are petechiae? What causes them?

A

Small, punctate hemorrhages

  • > typically due to decreased or abnormal platelets
  • > can also be due to increased intravascular pressure acutely -> choking someone to death
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28
Q

What are purpura and what causes them?

A

Slightly larger hemorrhages, typically due to vascular pathology (i.e. vasculitis)

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29
Q

What are hemorrhages in the subcutaneous tissue called?

A

Ecchymoses - bruises

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30
Q

What is the first thing that occurs to initiate hemostasis?

A

Transient arteriolar vasoconstriction

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31
Q

What is primary vs secondary hemostasis?

A

Primary - process of platelet adhesion, activation, and aggregation

Secondary - addition of coagulation cascade to be the “mortar” to the platelets’ “brick”

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32
Q

Normal endothelial cells do not want clotting to occur around them. When antiplatelet factors do they constantly release?

A
  1. Prostacyclin (PGI2) - vasodilator and inhibitor of aggregation
  2. NO - vasodilator
  3. ADPase - interferes with ADP for platelet aggregation
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33
Q

What are the anticoagulant defenses on endothelial cells.

A
  1. Heparin-like molecules - bind antithrombin 3 to mediate its inhibition of thrombin + others
  2. Thrombomodulin
  3. Tissue factor pathway inhibitor
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34
Q

How do thrombomodulin and tissue factor pathway inhibitor (TFPI) work?

A

Thrombomodulin -> binds thrombin, activates protein C and protein S -> degrades factors 5 and 8 which are needed for thrombin formation

TFPI - inhibits interaction between TF-7a complex and X

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35
Q

What fibrinolytic agent do healthy endothelial cells release?

A

Tissue-type plasminogen activator (tPA)

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36
Q

When endothelial cells are injured, what three compounds do they begin secreting?

A
  1. von Willebrand Factor - mediates platelet adhesion to ECM
  2. Tissue factor - pro-coagulant for the extrinsic pathway
  3. Anti-fibrinolytic - plasminogen activator inhibitors
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37
Q

What are the three phases of formation of the primary hemostatic plug?

A

3 A’s

  1. Adhesion
  2. Activation (Secretion)
  3. Aggregation
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38
Q

How does adhesion of platelets to the ECM work?

A

glycoprotein 1b (GpIb) receptors on platelets bind von willebrand factor on ECM, placed there by endothelial cells

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39
Q

What happens in platelet activation, generally? Include the skeleton of all processes.

A
  1. Alpha granules released
  2. Delta (dense body) granules are released
  3. Phospholipid complexes move the platelet surface -> needed for coagulation cascade
  4. Thromboxane A2 is synthesized -> promotes vasconstriction / aggregation
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40
Q

What is released from the alpha granules?

A

Alpha -> proteins including more vWF, factors 5 and 8 (inhibited by thrombomodulin), fibronectin for stickness, fibrinogen, and platelet factor 4 (inhibits heparin-like molecules)

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41
Q

What is released from the delta granules?

A

Calcium -> needed for coagulation cascade

ADP -> amplifies platelet activation / aggregation (blocked by clopidogrel)

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42
Q

What mediators enhance platelet aggregation in the aggregation phase of primary hemostasis/

A
  1. ADP (from delta granules)
  2. Thromboxane A2 (synthesized via platelets)
  3. Thrombin
  4. Fibrinogen
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43
Q

How does fibrinogen increase platelet aggregation?

A

Cross-links platelets via their GpIIb/IIIa receptors which are exposed during platelet activation (blocked by abciximab)

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44
Q

Where do the intrinsic / extrinsic pathway meet, and what is the process after this meeting point? Include cofactors as applicable

A

Both pathways meet with the activation of factor X to Xa

Prothrombin to thrombin: Xa uses Va as a cofactor to convert II to IIa

Fibrinogen to fibrin: IIa converts I to Ia (fibrinogen to fibrin)

Cross-linking of fibrin: Thrombin activates XIIIa (factor 13), which cross-links fibrin

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45
Q

How does the extrinsic pathway work and is this the vitamin K dependent pathway or no? Include cofactors as applicable

A

Tissue factor released by injured endothelium converts 7 to 7a an forms a complex

TF-7a complex activates factors IX and X to activate downstream pathways

-> note that activation of factor 9 is a bit of an overlap with the instrinsic pathway for activation of 10

YES - 2, 7, 9, and 10 are extrinsic pathway, depend on vitamin K

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46
Q

How is the intrinsic pathway initiated? What phase of the clotting does this occur vs extrinsic

A

Initiated by thrombin accumulation / activation of extrinsic pathway. Thus, this occurs in the amplification phase of the clotting. Extrinsic pathway is more of the initiation phase.

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47
Q

What exactly does thromin promote to get the instrinsic pathway going? What are the other amplification functions?

A

Amplifies conversion of 11 to 11a, 8 to 8a

Also:
Amplifies 5 to 5a (for factor 10) and
Activates 13 to 13a (for cross-linking of fibrin)

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48
Q

What is the sequence of the intrinsic pathway?

A

Hageman factor (12) is converted to 12a upon contacting collagen, converts prekallikrein to kallikrein and 11 to 11a

11a converts 9 to 9a with thrombin (2a) as an amplifier. (9 also activated by TF-7a)

Once 8 is activated to 8a via thrombin, 9a + 8a can convert 10 to 10a, feeding into the pathway.

Sequence is 12->11->9->10(conversion requires 8)

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49
Q

What is the overall role of thrombin in inflammation?

A
  1. Coagulation cascade -> amplifies multiple steps, makes fibrin and facilitates its crosslinking via 13a
  2. Platelets -> enhances activation and aggregation
  3. Endothelial cells -> binds receptors to stimulate leukocyte adhesion, has procoagulant and anticoagulant functions via thrombomodulin / heparin-like molecule
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50
Q

How does antithrombin 3 work? What enhances its activity

A

Inhibits thrombin and other coagulation factors

Activity enhanced by heparin-like molecule and heparins

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51
Q

What activates the protein C-S complex and what does it do?

A

Inactivates factors 5 (needed to make 2) and factor 8 (needed to make 10 from 9)

Activated by thrombin-thrombomodulin complex on endothelial cells

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52
Q

When is tissue-type plasminogen activator most effective?

A

When bound to fibrin (released by endothelial cells)

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53
Q

What is the purple collection tube for? Give the additive. What is it used for?

A

Whole blood (anticoagulated formed blood elements + plasma)

  • > EDTA is a strong irreversible sequesterer of calcium to prevent clotting
  • > used for CBCs and peripheral blood smears
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54
Q

What is the blue collection tube? Give the additive. What is it used for?

A

Plasma (supernatant of anticoagulated / whole blood)

  • > Contains clotting factors + serum
  • > additive is sodium citrate (reversibly binds calcium, enough calcium can be added to induce clotting)
  • > Used for coagulation tests like PT and aPTT
55
Q

What is the red collection tube for? How is it made? what is it used for?

A

Serum (plasma minus clotting factors)
Made by drawing out the liquid after the blood is clotted
-> Made in a glass tube without clotting activator (silica will spontaneously cause clotting)
or
-> plastic tube with clotting activator added

Used for serology (antibody tests) / routine chemistry

56
Q

How are platelets typically evaluated now?

A

Via platelet function assays
-> can test for abnormalities in primary hemostasis and platelet abnormalities

-> Can still get a count and an examination via a CBC or peripheral blood smear

57
Q

Why are the intrinsic / extrinsic pathways named the way they are? Which one is more important in vivo?

A

Instrinsic - contact activation -> requires only substances intrinsic to the vasculature

Extrinsic - requires things extrinsic to the vasculature normally (i.e. tissue factor, normally expressed in the ECM). However, it becomes expressed on endothelial cells during injury

Aka this makes minimal sense

Extrinsic more important in vivo

58
Q

What is added to perform a prothrombin time (PT)? What are we measuring

A

Citrated plasma + few platelets, tissue factor, phospholipid surface, and excess Ca+2 to overcome citrate
-> measure time it takes to form fibrin clot (in seconds)

59
Q

What three things can cause prolonged PT?

A
  1. Deficiency in vitamin K (needed for 2, 7, 9, 10)
    - > often due to warfarin or fat malabsorption
  2. Decreased synthesis of coag factors
  3. Increased consumption of coag factors (i.e. disseminated intravascular coag)
60
Q

What is the purpose of INR?

A

Standardization of prothrombin time between various labs which may use different tissue factors (international normalized ratio = INR)

61
Q

What is added to perform an activated partial thromboplastin time (aPTT)? What are we measuring?

A

Same citrated, platelet-poor plasma + silica contact activator + phospholipid + excess Ca+2 to reverse citrate

  • > only difference is contact activator instead of tissue factor
  • > check time it takes to form fibrin clot (measure of intrinsic pathway)
62
Q

What hereditary deficiencies in clotting factors would NOT cause an elevated aPTT?

A

Factors 7 and 13

-> not needed for instrinsic pathway

63
Q

Can vitamin K deficiency cause elevated aPTT?

A

Yes -> still needed for factor 9 in the intrinsic pathway, plus everything downstream to forming a clot

64
Q

Do anticardiolipin antibodies elevate aPTT and PT?

A

Yes -> they are antiphospholipid and interfere with this surface needed to form a clot (typically present on activated platelet)

65
Q

What is a thrombin time (TT)?

A

Time it takes to form a clot when thrombin + citrated, platelet-poor plasma + calcium are added

-> basically just that you can do fibrinogen to fibrin properly

66
Q

What two things can cause an elevated thrombin time?

A
  1. Deficiencies / defects in fibrinogen

2. Inhibitors of thrombin (i.e. heparin use, stops thrombin greatly in intrinsic pathway as well)

67
Q

What is a fibrinogen assay?

A

Test to see quantitative / functional abnormalities in fibrinogen

68
Q

What is Virchow’s triad?

A

The triad of interrelated factors leading to thrombosis, including

  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoagulability
69
Q

What are a couple examples of factors that can lead to endothelial injury predisposing to thrombosis?

A
  1. Atherosclerotic plaques
  2. Endocardial damage due to MI
  3. Inflammation
70
Q

Give the most common example of abnormal blood flow leading to thrombosis. How does this work / its most mechanism.

A

Venous thrombosis - due to stasis or turbulent rather than laminar flow
-> most commonly due to stasis (i.e. long flight or bedrest after a surgery)

71
Q

Can sickle cell anemia and aneurysms cause thrombosis? What class of pathogenic factors do they fall into within Virchow’s triad?

A

Yes -> fall into the abnormal blood flow due to turbulence (aneurysm) or stasis (sickle cell)

72
Q

What are the two types of hypercoagulability? How does their presentation differ?

A
  1. Primary (inherited) hypercoagulability
  2. Secondary (acquired) hypercoagulability

Differ in presentation because: younger patients will typically present with primary hypercoagulability

73
Q

Give examples of procoagulant and anticoagulant clotting factors which can be mutated to cause primary hypercoagulability.

A 
Procoagulant:
Factor 5 (Leiden) mutation -> cannot be lysed by protein C, no negative feedback via thrombomodulin

Anticoagulant:
AT3, protein C/S deficiences

74
Q

What amino acid precursor and clotting cascade factor mutation will cause primary hypercoagulation?

A
  1. Elevated homocysteine

2. Prothrombin mutation

75
Q

What type of disorder is heparin-induced thrombocytopenia and its pathogenesis?

A

Secondary hypercoagulability

Immune complexes form to platelet-factor 4 / heparin complexes (PF4 normally inactivates heparin-like molecules on endothelium).

These immune complexes bind platelets and increase activation, leading to a thrombocytopenia (more clots, more splenic clearance via opsonins) but overall increased clotting risk

76
Q

Why does estrogen predispose you to clotting?

A

Oral contraceptive use / hyper-estrogen states like pregnancy cause liver to makes more fibrinogen

77
Q

Do malignant neoplasms causing secondary hypercoagulability exist?

A

Yes - i.e. Trousseau syndrome

78
Q

What is the other syndrome which causes secondary hypercoagulability and is immune-complex mediated? What is the pathogenesis?

A

Antiphospholipid (anticardiolipin) antibody syndrome

Works by forming autoantibodies against phospholipids, not well understood because phospholipid surface is needed for clotting, but causes procoagulation in vivo.

79
Q

What are the two types of antiphospholipid antibody syndrome?

A
  1. Primary - occurs de novo (i.e. due to drug reaction or infection)
  2. Secondary - occurs secondary to another autoimmune disease like Lupus
80
Q

Other than recurrent clotting and low platelets, what is one diagnostic clinical feature of Antiphospholipid Antibody Syndrome?

A

Pregnancy complications (repeated spontaneous abortions, stillbirths, premature deliveries)

81
Q

How do you tell a post-mortem clot from a thrombus?

A

Postmortem clot - Not attached to vasculature, tends to have a dark layer and a light layer (serum vs formed blood elements settling)

Thrombus - Will be attached to vascular wall with lines of Zahn, more pronounced in arterial circulation. Also much more firm and homogenous

82
Q

What are lines of Zahn?

A

Evidence of blood flow in a clot

-> layers of platelets/fibrin (pale pink) alternating with layers of erythrocytes (dark red)

83
Q

Thrombi adherent to the walls of large chambers like heart and aorta are called? What is this the most common source of?

A

Mural thrombi

-> most common source of systemic thromboemboli

84
Q

What are vegetations?

A

Thrombi formed on heart valves

85
Q

What is venous thrombosis called?

A

Thrombophlebitis or phlebothrombosis

86
Q

What are the four possible outcomes of thrombus formation?

A
  1. Resolution / Dissolution
  2. Propagation
  3. Embolization
  4. Organization
87
Q

What is propagation?

A

Enlargement of thrombus at original site, usually with tail growing along the direction of blood flow

88
Q

What is embolization? Thrombus Vs embolus

A

Detachment or fragmentation of thrombi with travelling to a distant site
-> an embolus is just anything travelling to a distant site in the blood stream

89
Q

What is organization and how can blood flow be restored when the clot fully blocks the lumen?

A

Inflammation / ingrowth of granulation tissue, thickening of vascular intima, and forming a scar

Recanalization - process of capillaries in granulation tissue anastomosing and re-establishing blood flow THROUGH the thrombus

90
Q

What does arterial vs venous vascular obstruction cause?

A

Arterial - infarction (coagulative necrosis)

Venous - congestion and edema

91
Q

Where do arterial vs venous emboli end up?

A

Venous -> travels to lungs first

Arterial -> ends up in kidneys, spleen, brain, or extremities

92
Q

What is the general pathogenesis of disseminated intravascular coagulation (DIC) and what does it cause the patient to become susceptible to?

A

Massive activation of coagulation, forming widespread microthrombi, leading to consumption of platelets and coagulation factors

-> hemorrhagic diathesis

93
Q

What are the lab findings associated with DIC, and what is D-dimer?

A

Thrombocytopenia, and prolonged aPTT and PT

D-dimer = fibrin breakdown products due to fibrolysis, when plasmin breaks down fibrin linked by factor 13

94
Q

What is the most common consequence of a pulmonary thromboembolus?

A

Subclinical event -> dissolution or organization into a small intimal scar / fibrous web

95
Q

What determines whether a patient will have pulmonary hemorrhage, pulmonary infarction, or sudden death from a pulmonary thromboembolus?

A

Pulmonary hemorrhage - patient with good bronchial circulation to cover blood flow, but increased blood from systemic pressure -> destruction of alveolar septae (happens more in young people)

Pulmonary infarcation - smaller embolus but poor bronchial circulation -> not enough blood to save tissue (happens more in elderly)

Sudden death -> very large or saddle embolus blocking multiple airways, or many small emboli simultaneously
-> decreased blood to LV and drop in cardiac output leads to sudden death

96
Q

What can occur with chronic organization following repeated emboli?

A

Pulmonary hypertension

97
Q

Will pulmonary infarction secondary to embolus present with hemorrhaging?

A

Yes -> but the tissue will be infarcted because of Left-sided heart dysfunction leading to poor bronchial circulation. Overtime, however, that poor circulation will still bleed into that necrotic tissue

98
Q

How can a deep leg vein cause an arterial thrombus and what is this called?

A

Atrial or ventricular septal defect allows the thrombus to travel from venous to systemic circulation without passing the lungs

-> paradoxical embolus

99
Q

What type of embolus does long bone fracture put you at risk for? What is the usual clinical consequence?

A

Fat embolus

Usually - subclinical

100
Q

What is the most severe complication of a fat embolus? What is the classic presentation?

A

Fat embolism syndrome
-clinical triad: hypoxemia (respiratory difficulty due to pulmonary involvement), neurologic abnormalities, and petechial rash (due to thrombocytopenia from coated platelets)

101
Q

What are the common causes of air emboli?

A
  1. Sudden decreases in atmospheric pressure -> nitrogen gas which was once dissolved in blood precipitates out as gas bubbles
  2. Surgical / obstetric complications (IV, or during childbirth in contractions)
102
Q

What are the acute manifestations of decompression sickness?

A
  1. Bends - pain from air emboli within skeletal muscle and large joints
  2. Chokes - respiratory difficulty due to pulmonary injury
103
Q

What is chronic decompression sickness called and what does it cause?

A

Caisson disease

-> can cause long bone infarction when nitrogen bubbles block blood delivery

104
Q

How do amniotic fluid emboli arise and what do they typically cause?

A

Arise when amniotic fluid enters uterine veins, gets in lungs, and causes diffuse alveolar damage + DIC (from endothelial cells of baby seeding coagulation)

105
Q

What are the clinical findings of amniotic fluid emboli? How can it be diagnosed?

A

Similar to fat embolism syndrome
-> hypoxemia, neurologic abnormalities, and DIC (petechial risk can occur)

Diagnosed by seeing squamous cells and keratin from the baby (amniotic fluid) in pulmonary microvasculature

106
Q

What can cause cholesterol emboli?

A

Ulcerated atherosclerotic plaques -> visualized as cholesterol crystals

107
Q

What is the most common way to get bone marrow emboli?

A

CPR -> in adults, bone marrow is present only in axial skeleton (i.e. sternum, ilium) -> pressing chest during CPR can bone breakage and leakage

108
Q

Other than thrombosis and embolism, what are two other mechanisms of infarction in a tissue?

A
  1. Torsion / twisting of blood vessels -> i.e. mesentery or testicles, causing venous collapse and buildup of deoxygenated blood
  2. Extrinsic vascular compression -> i.e. herniation of mesentery or compression of vessels via neoplasm / edema fluid
109
Q

What is the definition of infarction?

A

A focal region of ischemic necrosis (usually coagulative)

110
Q

What causes a pale necrosis?

A

Arterial occlusion to an end-artery system in a solid organ (i.e. heart, kidney, spleen) -> no collateral circulation

111
Q

What does pale necrosis look like grossly / microscopically?

A

Grossly -> Pale, often pyramidal shaped area of necrosis with hyperemic margin

Microscopic - coagulative necrosis followed by scarring

112
Q

In order to make a timeline of infarction -> acute inflammation in coagulative necrosis -> early scar -> late scar, where should we examine the myocardium in MI?

A

Look at the periphery -> cells towards the middle will always be delayed before immune cells can get there

113
Q

What is the primary cause of hemorrhagic infarct, and what organs are most likely to develop this?

A

Venous obstruction -> leads to blood buildup in capillaries and hemorrhage into tissues

Common in tissues with dual blood supply / anastomoses: i.e. liver, lung, small bowel

114
Q

How can pale infarct become hemorrhagic infarct?

A

If pale infarction is re-perfused

115
Q

What is the gross and microscopic appearance of hemorrhagic infarct?

A

Gross - pyramidal shaped region most often, with rust-brown appearance

Microscopic - Coagulative necrosis with hemorrhage, along side numerous hemosiderin-laden macrophages from RBCs

116
Q

What do cerebral and septic infarcts cause? Include what causes septic infarct

A

Cerebral infarct - liquefactive necrosis

Septic infarct - abscess
-> caused by embolus with bacteria in it lodging somewhere

117
Q

What is the definition of shock?

A

Systemic hypoperfusion leading to widespread tissue hypoxia

118
Q

What is cardiogenic shock? When could this happen

A

Shock caused by decreased cardiac output.

Could be caused by MI, massive pulmonary embolism, or cardiac tamponade

-> decreased cardiac output

119
Q

What is hypovolemic shock? When could this happen

A

Shock caused by loss of blood or plasma volume

Happens in severe hemorrhage or burns which cause leakage of fluid out of skin + leaky vessels

120
Q

What is septic shock?

A

Shock caused by an overwhelming microbial infection (bacterial or fungal)

121
Q

Other than microbial endotoxins, what is responsible for the pathogenesis of septic shock? Include inflammatory mediators?

A

Host immune response

  • > inflammatory cells like PMNs / MACs
  • cytokines like TNF / IL-1
  • oxygen free radicals
  • > Complement activation
  • vasodilation and increased vascular permeability by C3a and C5a
  • C5a is chemotactic
122
Q

What is the direct effect of the immune cells in causing organ failure in septic shock?

A

Endothelial injury / activation

  • > Endothelium becomes prothrombotic and causes DIC
  • > vasodilation and increased vascular permeability also increases procoagulant effects (sludge in blood vessels)
123
Q

What are the metabolic derangements of septic shock?

A
  1. Acute phase responses like fever, left-shift, and APP
  2. Increased gluconeogenesis and decreased insulin to cause hyperglycemia
  3. Increased glucocorticoid production until fatty stores decrease and it drops
124
Q

What causes neurogenic shock?

A

Spinal cord injury leads to loss of vascular tone from loss of neuronal firing
-> blood pools peripherally and BP drops

125
Q

What are the three phases of shock which characterizes cardiogenic and hypovolemic shock?

A
  1. Nonprogressive phase
  2. Progressive phase
  3. Irreversible phase
126
Q

What happens in the nonprogressive phase of shock?

A

Lack of CO is compensated by neuronal / hormonal mechanisms

  • > increased SANS vasoconstriction / tachycardia
  • > fluid retention via RAA / ADH system
127
Q

What happens in the progressive phase of shock? Why? Think of skeletal muscle, kidney, and brain.

A

Widespread tissue hypoperfusion / hypoxia for a number of reasons

  1. Lactic acid builds and causes vasodilation
  2. Endothelium becomes injured -> DIC causing microthrombi, petechiae, hemorrhagic diathesis
  3. Renal hypoperfusion -> electrolyte abnormalities
  4. Cerebral hypoxia -> confusion
128
Q

What marks the irreversible stage of shock?

A

Systemic, irreversible cellular injury

129
Q

What does anaphylactic shock cause?

A

Type 1 hypersensitivity causes vasodilation and increased vascular permeability

130
Q

What does it look like in brain with ischemia / hypoxia?

A

Brain - red, dead neurons which die before glial cells

131
Q

What does it look like in heart with ischemia / hypoxia in shock specifically?

A

Contraction band necrosis

-> can see striations where muscles were contracting as they died due to catecholamine stimulation

132
Q

What dies first in kidney ischemia / hypoxia?

A

Proximal tubules -> acute tubular necrosis

133
Q

What is the “stress reaction” of the adrenal glands?

A

Decreased lipid in the cortex where the corticosteroids are made -> glucocorticoid synthesis will drop off late

134
Q

What is seen in the lungs during septic shock?

A

Diffuse alveolar damage due to inflammation in the capillaries

Pathobiology (20 decks)

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