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FTCM > L28, L30, L32, L34- Hemodynamic Disorders > Flashcards

L28, L30, L32, L34- Hemodynamic Disorders Flashcards

1
Q

breakdown the distribution of fluids in the body by percentages

A
  • TBW- 60% of body weight
  • 2/3 in ICF (40% of body weight)
  • 1/3 in ECF (20% of body weight): 3/4 in interstitium (15%), 1/4 in plasma (5%)
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2
Q

compare edema and effusion

A

Edema: fluid collection in interstitum / intercellular spaces Effusion: fluid collection in body cavities (pleural/lungs, pericardium, peritoneum)

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3
Q
  • pleural effusion = (1)
  • pericardial effusion = (2)
  • peritoneal effusion = (3)
A

1- hydrothorax

2- hydropericardium

3- ascites / hydroperitoneum

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4
Q

generalized severe edema is also called….

A

anasarca

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5
Q

list the 4 organs that can affect/cause edema and their associated symptoms

A
  • Heart: chest pain, dyspnea
  • Liver: jaundice, bleeding disorders
  • Kidney: urinary abnormalities, BP changes
  • GIT: nutritional deficiencies, diarrhea
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6
Q
  • the first classification edema is determining (1)
  • the morphology of edema is described as (2)
  • other possible consequences of edema are (3)
A

1- pitting or non-pitting

2- cell swelling, clearing / separation of ECM

3- impaired wound healing, thickening (skin), susceptible to infections

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7
Q

non-pitting edema is seen in…..

A
  • lymphatic obstruction
  • myxedema (severe hypothyroidism)

(pitting edema rules out these as contributing factors)

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8
Q

edema is classified by the following bases

A
  • mechanism
  • distribution: systemic/localized
  • clinicopathological conditions
  • content of accumulation: transudate v exudate
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9
Q

list the 4 mechanisms of edema

A
  • inc capillary hydrostatic P w/ Na retention
  • dec capillary oncotic P
  • lymphatic obstruction
  • inc membrane permeability
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10
Q

all lymphatics drain into (1), which drains all lymph fluid into (2) then (3) and finally returning to (4)

A

1- thoracic duct

2- L subclavian vein

3- SVC

4- circulation

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11
Q

Describe the 2 main causes of edema due to increased capillary hydrostatic pressure and whether it is local or generalized edema

A
  • generalized edema (usually, possibly localized in venous obstruction)
  • Impaired venous return: CHF*, venous obstruction due to thrombosis or venous compression due to external pressure (tumor)
  • Hypervolemia: Na retention secondary to renal failure
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12
Q

Describe the 3 main causes of edema due to decreased capillary oncotic pressure and whether it is local or generalized edema

A
  • generalized edema (usually)
  • Reduced albumin synthesis: liver disease, malnutrition
  • Inc albumin loss: renal diseases
  • Reduced GIT protein absorption: protein losing enteropathy, malabsorption, poor intake (Kwashiorkor)
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13
Q

Describe the 3 main causes of edema due to lymphatic obstruction and whether it is local/generalized and non-/pitting edema

A
  • localized, non-pitting edema (usually)
  • inflammatory (lymphadenitis)
  • neoplastic
  • post-surgical (dissection/removal) / radiation
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14
Q

Describe the 3 main causes of edema due to altered (or increased) membrane permeability

A
  • inflammation (acute/chronic)
  • angiogenesis
  • burns
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15
Q

describe the 2 types of CHF leading to edema and the differences in their presentation

A
  • RHF: inc capillary hydrostatic pressure –> peripheral edema (legs w/ standing, sacrum w/ bed ridden)
  • LHF: inc capillary hydrostatic pressure –> pulmonary edema (dyspnea, cough) ///// reduced GFR (due to low CO) –> RAS activation –> Na (+ H2O) retention
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16
Q

how is CHF induced edema managed

A
  • salt restriction
  • diuretics
  • aldosterone antagonists
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17
Q

describe Cirrohosis related edema

A
  • Portal HTN: inc capillary hydrostatic pressure in Splanchnic circulation => ascites
  • dec Albumin synthesis: dec capillary oncotic pressure
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18
Q

describe Renal Disease related edema

A
  • damaged basement membrane: protein loss (hypoalbuminemia) –> dec capillary oncotic pressure (Nephrotic syndrome)
  • Glomerulonephritis: generalized edema (peri-orbital edema); inflammatory glomeruli damage => dec GFR /// secondary hyperaldosterism (via RAAS) => Na/H2O retention
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19
Q

describe malnutrition related edema

A

-low proteins/AAs => dec albumin synthesis –> dec capillary oncotic pressure –> dec in effective plasma volume –> secondary hyperaldosteronism (via RAAS) –> Na/H2O retention => edema

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20
Q

Pulmonary Edema established (1) in intersitium and then (2) alveolar space. Its morphology is described as (3). The clinical symptoms of pulmonary edema include (4).

A

1- early phase (interstitial collection first)

2- frothy fluid in alveolar lumen

3- severely congested alveolar capillaries + alveoli filled with homogenous pink staining fluid

4- cough, dyspnea; in severe cases: frothy sputum, cyanosis

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21
Q

Describe Transudate by the following:

  • (1) process
  • (2) vascular permeability
  • (3) plasma protein leak
  • (4) protein content
  • (5) fibrin
  • (6) inflammatory cells
A

1- passive

2- normal vascular permeability

3- absent (protein leak)

4- protein <1.5g/dl / sp. gravity <1020

5- absent fibrin

6- absent inflammatory cells

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22
Q

Describe Exudate by the following:

  • (1) process
  • (2) vascular permeability
  • (3) plasma protein leak
  • (4) protein content
  • (5) fibrin
  • (6) inflammatory cells
A

1- active, inflammation

2- inc vascular permeability

3- proteins present

4- protein >1.5g/dl / sp. gravity >1020

5- fibrin present

6- inflammatory cells present

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23
Q

describe the 2 types of cerebral edema

A
  • Vasogenic: BBB disruption (instertitial edema), caused by infections, trauma, neoplasma
  • Cytotoxic: intracellular edema due to cell injury of gray matter, caused by hypoxia (CVA)
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24
Q

give the non-localizing and localizing symptoms of cerebral edema

A
  • Non-localizing: n/v, HA, papilledema (swollen optic nerve => mydriasis, impaired eye movements)
  • Localizing: specific motor/sensory deficiencies/abnormalities
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25
Q

cerebral edema is managed by…

A
  • IV mannitol (inc plasma osmolarity –> inc oncotic P)
  • steroids
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26
Q

describe the morphology of cerebral edema

A
  • flattened gyri
  • narrowed sulci
  • compressed ventricular cavities
  • midline shift
  • cerebral herniation
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27
Q

cerebral herniations are caused by (1) and have the following consequences, (2)

A

1- brain tissue displacement due to inc intracranial pressure

2- compromised blood supply, infarctions, edema

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28
Q

list the 3 common cerebral herniations

A
  • subfalcine (cingulate)
  • tonsillar
  • transtentorial (uncinate)
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29
Q

Subfalcine herniation is when (1) expansion displaces (2) found under (3). It will compress (4) leading to (5) injury of (6) and presenting with (7) as symptoms.

A

1- unilateral hemisphere expansion

2- cingulate gyrus

3- falx cerebri

4- ACA (anterior cerebral artery)

5- ischemic

6- primary motor/sensory cortex

7- weakness/sensory abnormalities in leg

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30
Q

Tonsillar herniation is when cerebellar tonsils are displaced through (1) leading compression of (2) and having (3) as important consequences.

A

1- foramen magnum

2- brainstem

3- compromised respiratory and cardiac centers => death

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31
Q

Transtentorial/Uncinate herniation is when (1) compresses against (2). This will compress (3) leading to (4) and compress (5). This herniation will put pressure on (6) leading to (7). It is also accompanies by (8)

A

1- medial temporal lobe

2- free margin of tentorium

3- oculomotor nerve (CN-III in midbrain: PSNS + motor)

4- mydriasis (PSNS) + impaired eye movements (motor)

5- PCA (posterior cerebral artery)

6- midbrain / contralateral cerebral peduncle

7- ipsilateral hemiparesis

8- Duret (flame shaped) hemorrhages in midbrain

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32
Q

untreated edema can lead to the following complications…..

A
  • impaired wound healing
  • thickening of skin
  • susceptible to edema
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33
Q

Net Filtration Pressure = ……

A

net filtration P = Hydrostatic P - Oncotic P

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34
Q

Hyperemia: definition, causes

A
  • ACTIVE inc blood volume in tissues
  • red color = oxygenated blood
  • caused by arteriolar dilation
  • Physiological cause: blushing, skeletal muscle in exercise
  • Pathological: inflammation
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35
Q

Congestion: definition, causes

A
  • PASSIVE inc blood volume in tissues
  • blue/red color = deoxygenated blood // usually comes with edema
  • impaired venous flow from tissues: cardiac failure, venous obstruction
  • ALWAYS pathological
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36
Q

Acute pulmonary congestion is caused by (1) with (2) and (3) as key features. Chronic pulmonary congestion has the following features: (4).

A

1- LHF

2/3- engorged alveolar capillaries, alveolar septal edema (frothy oozing fluid on gross appearance)

4- brown induration- hemosiderin laden macrophages = heart failure cells in alveolar space; thickened fibrous septa (>1 cell thick)

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37
Q

Acute hepatic congestion is caused by (1) with (2) and (3) as key features. Chronic hepatic congestion is also called (4), and has the following appearance, (5).

A

1- RHF

2/3- distended central vein and sinusoids due to blood; degeneration of central hepatocytes

4- nutmeg liver

5- central region (central vein) of lobule = reddish brown and depressed (centrolobular necrosis); surrounding zones = uncongested tan liver (near hepatic artery)

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38
Q

describe the microscopic features of the liver in chronic hepatic congestion (including the resulting complications)

A
  • centrilobular necrosis (reddish-brown color), near central vein [normal tannish areas surrounding central vein, near the hepatic arteries]
  • hemorrhage
  • hemosiderin laden macrophages
  • long standing cases: fibrosis (cardiac cirrhosis)
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39
Q

define a hemorrhage and its causes

A
  • extravasation of blood into exterior or nonvascular body space
  • BV damage OR defective clot formation
  • trauma, atherosclerosis, aneurysms, bleeding disorders, etc
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40
Q
  • (1) bleeding in pleural space
  • (2) bleeding in abdominal space
  • (3) bleeding in joint space
  • (4) bleeding in cardiac space
  • (5) bleeding in soft tissues (under skin)
A

1- hemothorax

2- hemoperitoneum

3- hemarthrosis

4- hemopericardium

5- hematoma

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41
Q

define petechiae, purpura, ecchymosis

A

1) Petechiae: pin point, 1-2 mm, hemorrhage in skin/conjunctiva, rupture of capillary or arteriole
2) Purpura: diffuse superficial hemorrhage in skin up to 1 cm diameter
3) Ecchymosis (bruising): larger superficial hemorrhage >1 cm

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42
Q

describe the progression of changes of extravasated blood (leading to color changes)

A
  • Hb, red-blue
  • bilirubin (Hb breakdown), blue-green
  • hemosiderin (further Hb breakdown), brown
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43
Q

(1) = blood in stool
(2) = vomiting blood
(3) = coughing blood

A

1- melena

2- hemetemesis

3- hemoptysis

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44
Q

what are the clinical features / implications of the following:

  • (1) minor petechiae
  • (2) recurrent hemorrhage
  • (3) severe hemorrhage
  • (4) brain stem hemorrhage
A

1- harmless

2- Fe deficient anemia

3- hypovolemic shock

4- death (small bleed in brain is way more detrimental then large bleed somewhere else in the body)

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45
Q

define DIC and name its types

A

DIC, disseminated intravascular coagulation: widespread small thrombi in microcirculation throughout body, accompanied by simultaneous bleeding (extensive microthrombi)

  • either acute, subacute, chronic
  • serious and often fatal
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46
Q

list the extensive causes of DIC

A

(disseminated intravascular coagulation)

  • Idiopathic
  • Diffuse endothelial injury: Gram-negative sepsis/endotoxin, viral, rickettsia, immunological injury (type II/III hypersensitivity, SLE)
  • Increased Thromboplastic Agents: amniotic fluid embolism, snake bite, promyelocytic leukemia, extensive tissue necrosis/burns, mucin, proteolytic enzymes from carcinoma
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47
Q

Endotoxins cause DIC by activating (1) via the release of (2) and (3). (2) and (3) act on endothelial cell surfaces in order to (4). Injured endothelial cells will induce (5).

A

1- monocytes

2- IL-1

3- TNF-α

4- inc Tissue Factor expression AND reduce thrombomodulin expression

5- platelet aggregation with activation of intrinsic pathway via collagen exposure

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48
Q

DIC has the following two main effects, (1) and (2). Diagnosis can be made by measuring levels of (3) and (4) in the blood.

A

1- dec tissue perfusion: shock, lactic acidosis, microinfarcts

2- bleeding: consumptive coagulopathy (used all platelets and clotting factors –> hemorrhage)

3- FDPs, fibrin degradation products

4- D-dimers

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49
Q

how do you manage DIC

A
  • heparin: prevents thrombi formation
  • replace platelets and plasma
50
Q

define Shock and list its types

A
  • generalized dec in perfusion to tissues, associated with reduced CO or reduced Blood Volume (cardiovascular collapse)
  • Cardiogenic, Hypovolemic, Septic, Distributive
51
Q

describe Cardiogenic Shock

A

Myocardial pump failure due to:

  • intrinsic myocardial damage (infarction), ventricular arrhythmias (dec contractility)
  • extrinsic compression (cardiac tamponade- fluid collection in pericardium)
  • outflow obstruction (pulmonary embolism- dec preload)
  • dec blood into arteriole vasculature and dec perfusion to tissues
52
Q

describe Hypovolemic Shock

A

Blood or Plasma volume loss due to: hemorrhage or fluid loss from burns. trauma, vomiting, diarrhea

53
Q

describe Septic Shock

A

Caused by systemic microbial infection: Gram+ infection, Gram- infection (endotoxic shock), fungi

-usually leads to diffuse vasodilation => dec overall tissue perfusion

54
Q

define Distributive Shock, and what are the two types

A
  • imbalance between compartments
  • Neurogenic or Anaphylactic
55
Q

describe causes of Neurogenic Shock

A

(a distributive shock)

  • fainting results from peripheral pooling of blood –> recumbent position from fall self corrects distribution –> inc venous return to restore CO
  • Anesthetic: loss of vascular tone, peripheral pooling
  • Spinal cord injury (=> vasodilation)
56
Q

describe Anaphylactic shock

A

(a distributive shock) IgE mediated response:

  • systemic vasodilation, inc permeability
  • reduced tissue perfusion
  • degranulation of mast cells / basophils => histamine, bradykinin, LTs
57
Q

list the effects of shock

A
  • hypotension
  • impaired tissue perfusion
  • cellular hypoxia
  • cell injury
  • cell death
58
Q

list the stages of shock with the associated cellular changes

A

1) initial non-progressive- cell adaptation
2) progressive- reversible injury
3) irreversible- irreversible injury

59
Q

The non-progressive stage of shock is considered the stage of (1) via (2). The following are the are the responders to decrease in blood pressure, (3). There is also generalized (4) throughout the body, with the following effects, (5).

A

1- compensation

2- reflex mechanisms

3- baroreceptors, catecholamine release, RAAS, ADH

4- SNS stimulation

5- tachycardia (baroreceptors), peripheral vasoconstriction (Epi./NE, RAAS), renal conservation of fluid (RAAS, ADH)

60
Q

During the non-progressive stage of shock the patient will appear (1) due to (2). The opposite is true, (3) appearance, in the (4) shock. (5) are less sensitive to SNS response and will maintain blood flow and oxygen delivery. (6) is a sign of non-progressive shock seen in blood work.

A

1- cool, pale

2- cutaneous vasoconstriction

3- warm, flushed (due to peripheral vasodilation)

4- septic shock

5- coronary and cerebral BVs

6- pre-renal uremia (elevated nitrogen species in blood, pre-renal failure)

61
Q

The progressive stage of shock is considered the stage of (1). There is an imbalance of (2). There is an elevation in (3) production by cells due to (4). Due to (3), the vasomotor response will become (5), causing (6) to occur. RBCs will start to (7). (8) are the key results from the progressive stage of shock and this is evident in a patient by the following signs and symptoms, (9).

A

1- impaired tissue perfusion

2- circulation and metabolic requirements

3- lactic acid (dec pH => lactic acidosis)

4- inc anaerobic glycolysis

5- blunted (less effective SNS response)

6- vasodilation (periphery)- arterioles dilate –> pooling blood into microcirulation (limbs collect blood)

7- sludge: aggregation on vessel walls –> dec blood flow

8- reduced CO, anoxic endothelial injury, DIC

9- confusion, dec urine output

62
Q

The irreversible shock is considered the stage of (1). There is widespread (2) with associated leakage of (3) to aggravate shock. Perfusion to (4) are at critical levels, and (5) is an additional factor that reduces CO. The kidney will undergo the following: (6). There is a failure of multiple organ systems, and in the GI, (7) can occur to worsen the shock. Survival is usually difficult even if hemodynamics are corrected.

A

1- decompensation

2- cell / tissue injury

3- lysosomal enzymes (=> necrosis)

4- brain, myocardium

5- myocardial depressant factor

6- ATN (acute tubular necrosis) –> ARF (acute renal failure) –> evident via renal uremia (inc nitrogen species)

7- ischemic bowel –> inc entry of bacteria => endotoxic shock

63
Q

In septic shock, there is systemic (1) leading to hypoperfusion. There is also activation of (2) that puts the body in a (3) state, allowing (4) to occur. (5) alterations lead to suppression of cell and tissue function. (6) is the net effect of the septic shock mechanism.

A

1- vasodilation

2- endothelial cells

3- hypercoagulable state

4- DIC

5- metabolic alterations

6- hypoperfusion + multiorgan dysfunction

64
Q

(1) is the most common cause of septic shock and (2) are the other possible causes. It is possible for these infections to remain (3) without detectable (4) and septic shock to still occur.

A

1- Gram+ bacteria

2- Gram- bacteria, fungi

3- localized

4- dissemination in blood stream

65
Q

describe the brief pathogenesis of septic shock (TSS)

A

(toxic shock syndrome)

1) superantigens (bacterial proteins, TSST-1) stimulate polyclonal T cell activation
2) T cells release high amount of CKs
3) diffuse rash, vasodilation, hypotension => death

66
Q

In septic shock, microbe will release mediators called (1) that activate (2) and (3) to induce a (4) response. (2) will release the following substances, (5), leading to the activation of (6).

A

1- PAMPs (pathogen associated molecular patterns)

2- inflammatory cells (PMNs, macrophages, dendritic cells)

3- complement

4- SIRS (systemic inflammatory response syndrome, note non-infectious agents can trigger this, ex. burns, trauma, etc)

5- CKs (TNF, IL-1), CK-like mediators (HMGB1, free oxy radicals), lipid mediators (PGs, PAF)

6- endothelial cells (via (5) mediators; IL-1, TNF are key)

67
Q

In the mechanism of Septic shock, the initial activation of endothelial cells causes the expression of (1) and the release of (2). (3) is also activated via PAMPs and (4), leading to the production of (5) to cause a pro-inflammatory state. In total endothelial activation will lead to the following, (6).

A

1- adhesins

2- second wave of CKs

3- complement

4- proteolytic activity of plasmin

5- anaphylotoxins (C3a, C5a), opsonins (C3b), chemotaxic fragments (C5a) [pro-inflammatory state]

6- thrombosis, DIC, inc vascular permeability, vasodilation

68
Q

In septic shock, DIC is a critical consequence. It results from pro-inflammatory CKs increasing (1) production and reducing (2) activity. (1) and (2) result from the increased expression of (3) and decreased expression of (4). (5) is also a contributing factors as it allows coagulation factors to aggregate, as they are not washed out.

A

1- TF (tissue factor)

2- fibrinolysis (clot destruction)

3- PAI (plasminogen activator inhibitor => dec plasmin, therefore less fibrinolysis)

4- TF pathway inhibitor, thrombomodulin, Protein C

5- reduced blood flow (stasis)

69
Q

list the results of septic shock initiated DIC (hint- 5)

A
  • systemic deposition of fibrin rich thrombi in small vessels
  • exaggerates hypoperfusion
  • consumes coagulation factors => bleeding
  • widespread vascular leakage and edema
  • deficient tissue nutrition and waste removal
70
Q

in septic shock, pro-inflammatory CKs cause increased vascular permeability by….

A

loosening of endothelial tight junctions by displacing VE-cadherins –> leaky vessels

71
Q

septic shock vasodilation is induced by the following mediators, (1), causing increased production of (2)

A

1- C3a, C5a, PAF (platelet activating factor)

2- NO => vasodilation / hypoperfusion

72
Q

In septic shock, there is (increased/decreased) insulin release with insulin (sensitivity/resistance) and therefore (hyper-/hypo-)glycemia. Because of this, (4) is initiated, which will compound (3). Being in a (3) state affects immune system via (5).

A

1- dec (insulin depression)

2- insulin resistance

3- hyperglycemia

4- gluconeogenesis

5- suppress bactericidal activity of PMNs + inc expression of adhesion molecules on endothelial cells

73
Q

describe Waterhouse Friderichsen syndrome

A
  • state of stress causes release of many mediators for vasoconstriction, and glucocorticoids are important
  • septic shock induces DIC
  • DIC causes adrenal necrosis
  • therefore a dec in glucocorticoids (after its initial surge)
74
Q

briefly describe how the following events in septic shock occurs: (1) immune suppression (2) organ dysfunction (3) reduced CO (4) ARDS

A

1- hyper-inflammatory state followed by immune suppression; hyperglycemia inhibits bactericidal activity, apoptosis of lymphocytes (spleen, lymph nodes)

2- dec delivery of O2, nutrients

3- high CK levels reduce myocardial contractility

4- (acute respiratory distress syndrome) inc vascular permeability and endothelial injury to lungs

75
Q

describe the treatment of septic shock

A
  • antibiotics
  • intensive insulin therapy (combat insulin sensitivity, hyperglycemia)
  • fluid replacement
  • physiological doses of corticosteroids (replace depressed levels after initial surge)

(experimental drugs to restore endothelial cell integrity)

76
Q

describe the changes in the brain during shock

A

Ischemic Encephalopathy:

  • edema: mottled discoloration of gray matter + gray-white junctions are blurred
  • watershed infarcts (ischemia to areas between ACA, MCA, PCA supply)
  • laminar cortical necrosis (follows gray-white junction, supplied by short penetrating arteries) + neuronal necrosis
  • hemorrhages (Pyramidal cells of hippocmpus, Purkinje cells of cerebellum are critical)
77
Q

describe the changes in the heart during shock

A
  • focal and widespread necrosis
  • contraction band necrosis (lack of nuclei - dead cells)
78
Q

describe the clinical features of shock

A
  • weak rapid pulse
  • tachypnea
  • cool clammy cyanotic skin (warm, flushed in septic)
  • gradual cardiac, cerebral, pulmonary dysfunction
  • electrolyte disturbances, metabolic (lactic) acidosis
  • renal failure
  • MIs, bleeding, sepsis – life-threatening
79
Q

briefly describe pathogenesis of thrombosis

A

Virchow’s Triad:

1) endothelial injury –> (2), (3)
2) abnormal blood flow –> (1), (3)
3) hypercoagulability via (1), (2)

80
Q

list some common causes of endothelial injury (predisposing one to thrombus formation)

A

(arterial thrombi)

  • stress via HTN
  • bacterial toxins (in shock)
  • hypercholesterolemia
  • homocytinuria
  • cigarettes (CO)
81
Q

Loss of laminar flow in blood vessel occurs due to (1) or (2) causing (3) blood flow; this is termed (4).

A

1- vasodilation

2- structural vascular damage (atherosclerotic plaques)

3- turbulent flow

4- stasis

82
Q

list the effects of blood stasis

A
  • endothelial cell hypoxia / damage
  • inc platelet contact with endothelium + local activation of coagulation factors —> platelet/fibrin build-up
  • build-up is contributed by prevention of activated clotting factor dilution + reduced flow of clotting inhibitors
83
Q

list the Hereditary components that lead to hypercoagulability

A

(lack of natural anti-coagulants)

  • Factor V mutation, Leiden mutation (most common)
  • Anti-thrombin III deficiency
  • Protein C and S deficiency
84
Q

list the diseases of states that lead to Acquired hypercoagulability

A
  • terminal cancer: Trousseau’s syndrome- necrotic tumors release thrombogenenic substances
  • cardiac failure: anoxic tissue damage leads to thrombogenic substance release
  • severe trauma, burns
  • oral contraceptives: inc clotting factor production
85
Q

Thrombus:

(1) platelet involvement?
(2) location
(3) color
(4) consistency
(5) attached to vessel wall?
(6) Lines of Zahn?

A

1- platelets involved

2- occurs only inside vessels

3- red (venous) OR pale (arterial)

4- firm

5- attached to vessel wall

6- has line of zahn

(3 parts: platelets, endothelium, fibrin deposition / blood coagulation)

86
Q

Clot:

(1) platelet involvement?
(2) location
(3) color
(4) consistency
(5) attached to vessel wall?
(6) Lines of Zahn?

A

1- no platelets involved (fibrin is only component)

2- occurs outside of vessels: test tube, hematoma [inside vessels postmortem]

3- red

4- gelatinous

5- not attached to vessel wall

6- no lines of zahn

(1 part: fibrin collection)

87
Q

describe Lines of Zahn

A

(only present in thrombus, not clot)

alternating pale and dark lines

  • pale = platelets, fibrin
  • dark = RBCs
88
Q

list the sites of arterial thrombosis and indicate the type of blockage usually associated

A
  • Heart, mural
  • Aneurysm, mural
  • Aorta, atherosclerotic plaque
  • Other arteries, occlusive: coronaries (most common), carotids, cerebral, femoral, mesenteric
89
Q

describe the features of venous thrombosis

A
  • takes shape of vessel (in which it forms)
  • redder than arterial thrombus (pale) due to more RBC content
  • Varicosities (superficial leg veins) rarely embolize
  • 90% in deep veins of leg: deep calf veins (at or above knee) include femoral, popliteal, iliac
90
Q

describe the clinical features of a DVT

A

(affecting deep leg veins)

  • foot and ankle edema, pain, tenderness
  • 50% asymptomatic (due to collateral supply)
  • high embolism risk
  • Trousseau’s Syndrome: unexplained thrombophlebitis (vein inflammation related to thrombus), recurrent (observe for underlying abdominal malignancy, ex. pancreatic CA => release of procoagulants)
91
Q

describe the effects of an arterial thrombus on an organ

A

Acute => infarct

Slow => atropy, fibrosis

Heart => systemic emboli

92
Q

describe the effects of venous thrombus on organs

A
  • edema, congestion
  • Rarely: Pressure of edema –> secondary block of artery => infarction
  • pulmonary emboli
93
Q
  • the most common origin of thrombi are in (1) and it usually embolizes to (2)
  • the most common clinically significant thromboemboli arise from (3) and embolize to (4)
A

1- deep leg veins

2- lungs (mostly asymptomatic)

3- heart (80%)

4- lower extremities (75%), brain (10%- CVA)

94
Q

(1)% on emboli result from (2)

other emboli include the following: (3)

A
  • 99% are thromboemboli (dislodged thrombus)
  • Others: fat, air/gas bubbles, bone marrow, tumor cells, amniotic fluid, atherosclerotic plaque debris, foreign body
95
Q

Pulmonary thromboembolisms are found in (1)% of all autopsies and present clinically as (2). They mostly originate from (3). They are also responsible for (4)% of deaths in hospitalized patients.

A

1- 65%

2- asymptomatic

3- deep leg veins

4- 15%, usually the occurs the first time they get out of bed (immobilization –> start to move –> calf muscles dislodge large thrombus –> PE at pulmunary trunk)

96
Q

classify the types of pulmonary embolisms

A
  • Massive: sudden obstruction to 60% of pulmonary vasculature => sudden death (no time to develop infarction)
  • Major: multiple medium size vessels occluded –> only 10% infarction (b/c heart disease) due to collateral circulation in bronchial arteries => dyspnea, cough
  • Minor: small vessels obstructed, emboli is lysed, asymptomatic

[recurrent pulmonary emboli –> pulmonary HTN)

97
Q

Systemic thromboembolisms are defined as emboli that travel in (1). There sites of origination include (2), (3), (4). They usually emobolize to (5) or (6) causing (7).

A

1- arterial circulation

2- heart, mural (80%)

3- aorta, ulcerated atherosclerotic plaque

4- venous circulation, paradoxical embolism b/c it travels thru ASD or VSD in heart (skips pulmonary circulation)

5- lower extremities (75%)

6- brain (10%)

7- infarction, due to blocking an end artery

98
Q

Fat embolism syndrome is characterized by the following symptoms….(include time of onset)

A
  • pulmonary insufficiency, neurological Sxs (irritability, restlestness –> progression to delirium/coma), anemia, thrombocytopenia
  • 1-3 days after injury: sudden onset of tachypnea, dyspnea, tachycardia, petechiae

(fatal 10% of the time)

99
Q

describe how to diagnose fat embolisms

A
  • sputum or urine samples
  • mostly post-mortem (must use frozen tissue sections, as traditional alcohol prep will dissolve fat)
100
Q

Air embolisms originate into (arterial/venous) circulation through the following methods, (2). Only a total volume of (3) air causes death as bubbles coalesce to cause (4).

A

1- venous circulation

2- neck wounds, thoracocentesis, cut in IJV, hemodialysis (child birth, abortion)

3- 150 mL

4- physical obstruction of blood flow in RV, lungs, brain

101
Q

describe Nitrogen Embolism (and its alternate names)

A

(the bends, Caisson’s disease)

  • Deep Sea diving w/o Caisson’s chamber OR Scuba diving (deeper than 10m)
    1) O2/N2 dissolve in blood/tissues due to high P (high amounts)
    2) sudden resurfacing => O2 reabsorbed, N2 bubbles out => ruptures tissues and emboli formation in vessels
    3) platelets adhere to N2 –> secondary thrombi, to aggrevate ischemia
    4) affects brain (death), muscles, joints (bends), lungs (edema, hemorrhage => choking)
102
Q

(1) is the more chronic form of N2 embolisms, with persistent gas emboli in (2). This leads to (3). Treatment includes (4).

A

1- Caisson’s disease

2- bones

3- necrosis of femur, tibia, humerus (long bones)

4- pressure chamber, slow decompression

103
Q

(1) is an embolism in small pulmonary vessels after vigorous cardiac resuscitation and causes (2)

A

1- bone marrow embolism

2- nothing, incidental finding on autopsy, not a cause of death

104
Q

Amniotic fluid emobolism occurs due to (1) and usually consists of (2) and will lodge into (3). It will cause (4).

A

1- after labor

2- squames (dead skin flakes), hair, meconium (1st BM)

3- pulmonary vessels

4- usually fatal: DIC, pulmonary edema, diffuse alveolar damage

105
Q

describe the event of an atherosclerotic emboli and its associated symptoms

A

(usually incidental finding on autopsy)

  • small dislodged fragments from main renal artery atherosclerosis –> smaller intrarenal branches => small infarcts
  • no clinical Sxs (rarely infarction)
106
Q

Foreign Body emboli usually originate from (1)

Infective emboli usually cause (2)

A

1- cotton fibers, catheters (incidental findings)

2- infarcts, mycotic aneursym

107
Q

define infarction and its most common cause

A
  • ischemic necrosis caused by arterial occlusion or occlusion of venous drainage
  • 99% results from thrombotic OR embolic events
108
Q

The main cause of infarctions is (1), other causes include (2), (3), (4), (5)

A

1- thrombus, embolus

2- hemorrhage in atherosclerotic plaque

3- vessel torsion: venous, arterial, or both

4- hypoperfusion: secondary to MI, severe hemorrhage, septic shock

5- vasculitis: rupture, thrombosis

109
Q

White infarcts:

(1) little or large amount of bleeding
(2) affected organs
(3) arterial or venous occlusion
(4) duel or single blood supply

A

(appears white or pale)

1- little bleeding

2- solid organs: kidney, spleen, heart

3- arterial occlusion

4- single blood supply

110
Q

Red infarcts:

(1) little or large amount of bleeding
(2) affected organs
(3) arterial or venous occlusion
(4) duel or single blood supply

A

1- large amount of bleeding

2- soft organs (with tissue spaces): lungs, SI

3- venous occlusion (congestion –> infarction)

4- duel blood supply (lungs, SI): bleed from anastomosing vessels

(note- can also occur whenflow is reestablished after arterial occlusion or necrosis)

111
Q

desribe the Gross, Microscopic, and Septic appearance on infarcts

A

Gross: wedge shape (occluded vessel at apex), initial congestion with ill defined margins –> well-defined, rim of hyperemia –> brown color due to hemosiderin

Micro: ischemic coagulation necrosis

Septic: abscess formation

112
Q

list the factors that influence infarction development

A
  • nature of vascular supply (single, duel)
  • rate of development of occlusion: sudden is dangerous –> infarction, slow –> ischemia, fibrosis
  • vulnerability of tissue to hypoxia: brain is highly vulnerable, bone/muscle are not
  • O2 carrying capacity of blood: anemia
113
Q
  • dual blood supply (inc/dec) chances of infarctions; this is evident in the following areas: (2)
  • collateral circulation (inc/dec) chances of infarctions
A

1- decreases chances

2- lungs, liver, circle of willis (brain), hand (ulnar/radial art.)

3- decreases chances: enlarged anastomoses in coronary circulation reduces risk

114
Q

The following veins have no collateral supply, (1). Therefore a venous block in any of (1) will lead to (3) followed by (4) and then (5).

A

1- SVC, central retinal vein(/artery), superior sagital sinus, renal veins, cavernous sinus

2- venous block => edema, hemorrhage, congestion

3- secondary arterial block due to hydrostatic pressure

4- infarction (hemorrhagic)

115
Q

Infarction:

  • (1) cells are the initial infiltrators
  • (2) are the secondary infiltrators
  • (3) is the result of (1) followed by (2)
A

1- PMNs, macrophages

2- granulation tissue, lymphocytes, plasma cells

3- scar formation (contraction)

116
Q

describe the requirements and the appearance for a pulmonary infarction

A

1) pulmonary thromboemboli of medium size
2) compromised bronchial circulation OR cardiac failure

(if just (1) –> hemorrhage, no infarction)

Morphology: red infarction, base towards pleura, 75% in lower lobes, fibrous exudate on pleura

117
Q

Cerebral infarct are more commonly caused by (1) via (2) or sometimes (3). Another cause includes (4) which are (5) sites.

A

1- embolism

2- cardiac mural thrombi (MI, AFib)

3- carotids

4- thrombotic occlusions (atherosclerosis)

5- carotids, MCA origin, either end of basilar artery

118
Q

describe the progression of cerebral infarcts

A

12 hrs: coagulation necrosis begins –> softening, color changes; possible hemorrhage due to reperfusion

48 hrs: edema of infarcted region, acts as intracerebral massed –> inc intracranial pressure // microglial engulf necrotic material => Gitter cells

Later: further tissue breakdown and softening –> liquefactive necrosis, cyst formation, overylying meninges thickened, surrounding gliosis regions

119
Q

A MI is described as (1), where the (2) vessel is most commonly involved. (3) necrosis occurs and the heart appears (4). (5) is raised in serum. Patients present with (6).

A

1- coronary atherosclerosis with superimposed thrombosis

2- LAD

3- coagulation necrosis

4- blotchy (initially) –> pale scar (later)

5- cardiac enzymes (CK-MB, TnT, TnC)

6- severe chest pain / angina

120
Q

describe why venous and arterial thrombi have different colors

A

Venous = red due to slower flow and therefore more RBCs are apart of the thrombus

Arterial = gray due to faster flow and therefore less RBSs are apart of the thrombus

121
Q

describe thrombus growth/progression

A
  • propagation: growth along vessel towards the heart
  • breaks apart –> emboli
  • organize (occlusion) –> recanalization –> apart of new vessel wall (although has smaller vessel caliber)
  • completely dissolve
122
Q

Fat emboli start with (1) allowing (2) to enter circulation. Their pathogenesis includes (3) and (4).

A

1- trauma to bone, subcutaneous tissue, burns

2- fat globules (via rupture of marrow vascular sinusoids or ruptured venules)

3- mechanical blockage: globules enlarge as platelets adhere

4- biochemical injury: free FAs released from adipose tissue –> toxic to endothelial cells –> DIC, clogged pulmonary and systemic capillaries

FTCM (16 decks)

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