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General Pathology -- Roecker > Gen Path. Exam 2 Section 3: Hemodynamic Disorders, Thromboembolism, and Shock > Flashcards

Gen Path. Exam 2 Section 3: Hemodynamic Disorders, Thromboembolism, and Shock Flashcards

1
Q

Hemodynamic

A

flow of blood within organs and tissues; related to issues associated with blood flow

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2
Q

Hemostasis

A

appropriate clotting of blood without causing excessive clotting

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3
Q

Thrombosis

A

formation of a blood clot within a vessel

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4
Q

coagulation

A

used to describe physical change of blood at site of thrombosis; blood is transitioning from fluid to a semi-solid or gel-like state

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5
Q

Thrombus

A

“blood clot”; final product of thrombosis

Ex: Deep Vein Thromboses (DVT)

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6
Q

Factors that increase risk of Thrombus

A

obesity, immobility, family history, older age (>50), chronic inflam., pregnancy, smoking, dehydration, advanced cancer, trauma, surgery, diabetes, conditions causing hypercoagulable state

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7
Q

Embolus

A

unattached mass traveling through bloodstream (is the mass that causes an embolism)

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8
Q

Embolism

A

when embolus causes a blockage in blood flow

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9
Q

Thromboembolism

A

general term; combines thrombus & embolism; describes vascular blockage by piece of material that broke loose from a thrombus (clot); results in obstruction of blood (many times in venous flow)

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10
Q

Hematoma

A

localized collection of blood within body, outside of blood vessels; commonly due to trauma
Exs: Epidural Hematomas & Subdural Hematomas

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11
Q

Hemorrhage

A

“bleeding”; more precisely describes profuse amount of blood loss from ruptured blood vessel
Examples: postpartum hemorrhage, ass. with severe trauma (MVA or gunshot)

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12
Q

What are the most common hemodynamic disorders in the U.S. causing morbidity and mortility?

A 
myocardial infarction (heart attack) 
cerebral infarction (stroke)
pulmonary embolism (P.E.)
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13
Q

Hyperemia

A

increase in amount of blood within a tissue; and ACTIVE process that involves vasodilation to increase tissue blood volume; occurs at ARTERIOLES

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14
Q

Why does hyperemia occur?

A

as a vascular component of acute inflammation OR as a method to deliver more blood to body’s surface to regulate body temp.
–will engorge skeletal muscle tissue with increase blood when working out OR will engorge GI tract with blood to assist in digestion

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15
Q

Congestion

A

increase in amount of blood within a tissue; PASSIVE process from impaired VENOUS outflow; commonly manifest with cyanosis and transudate edema; more likely to experience hypoxia

Examples: Chronic Pulmonary Congestion & Congestive Hepatopathy

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16
Q

What two things can produce congestion?

A

Deep Vein Thrombosis (DVT) = produces congestion in isolated single region of body (lower leg, ankle)

Congestive Heart Failure (CHF) = produces systemic (body-wide) congestion –> in lunges and rest of body

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17
Q

Chronic Pulmonary Congestion

A

most likely results from CHF; causes pulmonary capillaries to engorge –> injures them –> and fibrotic changes in alveolar septa –> bleeding within lungs

  • dyspnea (due to edema + congestion)
  • “heart failure cells”
  • hyrdothorax
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18
Q

hydrothorax

A

fluid (edema) accumulates in lungs within plural space (within pleural cavity)

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19
Q

“heart failure cells”

A

when macrophages become engorged with hemosiderin

- occurs in pulmonary alveolar macrophages due to injury that caused inflammation

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20
Q

Congestive Hepatopathy

A

“chronic passive liver congestion”; result from any condition inhibiting venous blood outflow form liver; manifests with “centrilobular necrosis” AND macrophages overloaded with hemosiderin
- “nutmeg liver”

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21
Q

Common Causes of Congestive Hepatopathy

A

cirrhosis (from alcohol liver disease, NEFLD, chronic inflam.)
liver cancer and metastasis cancer to liver
large blood clots within liver

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22
Q

Edema

A

= accumulation of excess interstitial fluid; common feature of tissue congestion

  • Anasarca
  • Hydrothorax
  • Ascities
  • Dependent Edema
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23
Q

Anasarca

A

accumulation of body-wide subcuatneous edema; commonly from–> liver failure, sever malnutrition, heart failure, kidney failure

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24
Q

Ascites

A

edema within peritoneal cavity; Occlusion of hepatic veins due to:

  1. cirrhosis
  2. cancer, blood clots, etc.
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25
Q

Dependent Edema

A

gravity-dependent; pulls edema to lowest point in body

  • If can sit or stand: edema in lower legs or ankles
  • If unable to sit: edema in soft tissues posterior to sacral region
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26
Q

Exudate vs Transudate

A

Exudate: protein-rich, inflammatory, no pitting, osmosis

Transudate: protein-poor, non-inflammatory, pitting, no osmosis

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27
Q

Two opposing forces that regulate movement of fluid form blood vessels to interstitium:

A
  1. Intravascular Hydrostatic Pressue

2. Osmotic Pressure of blood’s plasma

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28
Q

5 Contributing Factors to Edema

A
  1. Increased Hydrostatic Pressure
  2. Reduced Plasma Osmotic Pressure
  3. Lymphatic Obstruction
  4. Sodium and Water Retention
  5. Acute Inflammation
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29
Q

Increased Hydrostatic Pressure

A

most commonly due to obstructions in VENOUS drainage

  • in isolated areas: commonly due to DVT
  • body wide: commonly due to impaired venous drainage to heart (in CHF)
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30
Q

Congestive Heart Failure

A

progressively worsening condition (heart inadequately pumps blood–> blood congests in lungs–> then to rest of body’s veins –> therefore increase hydrostatic pressure –> transudate accumulate in tissues)
- DOES NOT provided adequate blood to kidneys–> activates RAAS (renin-angiotensin-aldosterone system)

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31
Q

Renin- Angiotensin- Aldosterone System (RAAS)

A

when kidney’s do not get enough blood; results in increased re-absorption of NA and therefore hold onto more water via osmosis–> increase body’s total blood volume–> adds additional workload to already failing heart
(creates positive feedback loop of increased edema)

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32
Q

Reduced Plasma Osmotic Pressure

A

causes anasarca; decrease in protein content of blood

- Hypoalbuminemia

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33
Q

Hypoalbuminemia

A

= low albumin in blood; used synonymous with low plasma protein levels
Caused by: Nephrotic Syndrome or Liver Disease

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34
Q

Nephrotic Syndrome

A

lose plasma proteins to external env. via urination; main mechanism is damage to glomeruli of kidney due to kidney damage (from diabetes, Lupus, or amyloidosis)

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35
Q

Liver Disease

A

lack of plasma protein synthesis; Protein Malnutrition–may inhibit liver’s ability to synthesize plasma proteins = “protein-energy malnutrition” or Kwashiorkor

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36
Q

Lymphatic Obstruction (related to edema)

A

results in accumulation of lymph within lymphatic systems = lymphedema

  • Elephantiasis
  • Breast Tumors
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37
Q

What are the most common reasons for Lymphedema?

A
  • fibrosis form chronic inflammation
  • local tissue distortion form trauma or surgery
  • neoplastic obstruction form benign or malignant tumor
  • (ionizing radiation, infection)
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38
Q

Elephantiasis (Filariasis)

A

result of lymphatic filariasis infection (a parasitic worm known as Wuchereria bancrofti); attacks inguinal lymphatic vessels and causes lymphatic fibrosis
- common infection in tropical areas and endemic to: Africa, Asia, and Pacific island nations

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39
Q

Breast Tumors (related to lymphatic obstruction)

A

create neoplastic invasion; benign or malignant–> may compress/invade axial lymph nodes or lymphatic vessels
Common Results:
- inverted nipple
- Peau d’orange (dimpling)
- possibly lymphedma of upper extremity that is drained by obstructed lymph nodes (could be after a mastectomy or radiation too)

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40
Q

Sodium and Water Retention (related to edema)

A 
increase NaCl- (salt) --> increase water due to osmosis --> increase blood volume --> increase hydrostatic pressure 
Conditions That May Cause This:
- excessive salt intake
- acute renal failure
- poststreeptococcal glomerulonephritis
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41
Q

Acute Inflammation (related to edema)

A

from increase vessel permeability due to: infection, injury, allergies, etc.; will be exudate edema

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42
Q

Hemorrhage

A

= “extravasation” or “bleeding” –> when blood moves from inside blood vessel and into external tissues or external env.

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43
Q

What is a hemorrhage frequently associated with?

A
  • mechanical trauma, invasion of tumor, vascular injury, or loss of normal clotting capabilities (problems with hemostais)
  • chronic tissue congestion –> hemorrage in capillaries
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44
Q

Hematoma

A

= when hemorrage results in blood within a tissue; “bruise”

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45
Q

Severity of a hemorrage involves what 3 things

A
  1. rate of blood loss
  2. total volume of blood lost
  3. site where hemorrhage is occuring (i.e. in cranium or thigh)
    - Hypovolemic shock = lethal; occur w/ acute loss of >20% of total blood volume
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46
Q

Internal Hemorrhage

A

hematoma; macrophages capture iron and body reuses it for erythropoiesis

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47
Q

External Hemorrhage

A

blood lost to external env.; iron UNABLE to be reused; more likely to deplete iron stores–> result in iron-deficiency anemia (IDE)

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48
Q

Common causes of External Hemorrhage

A
  • peptic ulcer disease
  • colon polyps
  • colorectal cancer
  • heavy menstruation
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49
Q

Petechiae

A

very small areas of hemorrhage; ~1-2mm on skin, mucosa, or serosal surfaces
Common Causes: low platelets (thrombocytopenia), Vit. K deficiency, vessel fragility form Vit. C deficiency

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50
Q

Purpura

A

slightly larger hemorrage than petechiae; ~3-5mm

Common Causes: mechanical trauma, vasculitis, vessel fragility from Vit. C deficiency. Kaposi Sarcoma (AIDS)

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51
Q

Contusion vs Ecchymoses

A

contusion = result of trauma
ecchymoses = results of trivial trauma (MC due to patient taking Aspirin, Warfarin, or have Vitamin deficiency)
BOTH: bruises, > 1 cm, transition from:
reddish blue –> blue-green –> yellow brown
hemoglobin –> bilirubin –> hemosiderin

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52
Q

Hemostasis

A 
adequately clotting blood
Involves:
1. endothelial cells
2. platelets 
3. coagulatin cascade
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53
Q

Primary Hemostasis

A

when platelets aggregate on vessel wall –> following endothelial damage; von Willebrand Factor (vWF) and collagen are exposed to elements of blood
- when platelets contact vWF–> they become “activated” and form initial “primary hemostatic plug”

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54
Q

Secondary Hemostasis

A

formation of fibrin-rich clot
injury to vascualr endothelia exposes tissue factor–> activates series of rxns –> finalized with thrombin–> which cleaves fibrinogen into fibrin (an insoluble protein)–> produces fibrin-rich mesh –> more permanent clot

55
Q

Coagulation cascade

A

a complex series of enzymatic rxns that assist formation of fibrin-rich clot, via formation of thrombin (to cleave fibrinogen to fibrin)

56
Q

Thrombosis and Virchow’s Traid

A

3 Primary Abnormalities that Cause Intravascular Thrombosis:

  1. endothelial injury
  2. abnormal blood flow
  3. hypercoagulability
57
Q

Endothelial Injury (Virchow’s Traid)

A

primary cause of thrombosis in heart or arterial system; exposes vWF and tissue factor –> promote thrombosis; causes “endothelial activation” = anti-thrombotic endothelia to become pro-thrombotic

58
Q

Stimuli that May Cause Endothelial Injury

A
  • atherosclerotic plaques
  • inflammation
  • abnormal blood flow
  • hypercholesterdemia
  • toxic exposure (i.e. chemicals enter blood after smoking tobacco)
59
Q

Abnormal Blood Flow (Virchow’s Traid)

A

common to area of blood turbulence OR slow blood flow (stasis); common to VEINS

60
Q

Stimuli that Produce Abnormal Blood Flow

A
  • obesity, inactivity
  • varicosities, aneurysms
  • arrhythemia
  • cardiac valve stenosis
  • atherosclerotic plaques
  • Polycythemia and Sickle Cell Disease
61
Q

Hypercoagulability (Virchow’s Traid)

A

someone has an abnormal high tendency for clot formation; GENETIC disorder that may result in abnormal clotting proteins (Factor V or Prothrombin Mutation), but can also acquire it

62
Q

Factor V Mutation

A

common; ~ 2-10% all Caucasians; increase likelihood of thrombosis by causing Factor V amino acid to be less active–> inhibits normal anti-thrombotic mechanism; increase risk of clotting up to 50-fold

63
Q

Prothrombin Mutation

A

(prothrombin thrombophilia); produces an increased risk of cloting 3-5 fold; present in ~1 in every 50 people
Prothrombin–normally serves as pro-thrombotic protein–> when mutated–> it increase inds. tendency to form clots

64
Q

Secondary (acquired) Hypercoagulability

A

develops when ind. acquires an increased clotting risk later in life following:
- obesity, smoking, oral contraception, conditions causing increased estrogen levels, advanced cancer, vascular congestion (CHF)

65
Q

Growth of Thrombi

A
  • grow toward the heart
    1. Arterial Thrombi: grow “retrograde” direction; against direction of blood flow
    2. Venous Thrombi: grow “anterograde” direction, grow with blood flow
66
Q

Fate of Thrombus

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and Re-canalization
67
Q

Propagation (Fate of Thrombus)

A

thrombus enlarges via accumulation of additional platelets and fibrin proteins; likelihood of vascular obstruction or emboization increase proportionally

68
Q

Embolization (Fate of Thrombus)

A

when part or all thrombus dislodges; travels until gets stuck; usually in capillaries

69
Q

Dissolution (Fate of Thrombus)

A

if fibrinolytic factors produced by body dissolve thrombus; include t-PA (tissue plasminogen activator) or heparin

70
Q

Organization and Re-canalization (Fate of Thrombus)

A

could occur in older thrombi; endothelia, smooth muscle cells, and fibroblasts fill in area of clot–> in time capillary channels may form

71
Q

Clinical Features of Venous Thrombi

A
  • most common
  • may cause tissue congestion, pitting edema, and tenderness
  • much less lethal than arterial thrombi
  • primary concern–> is potential to embolize to lungs (P.E.) and cause a pulmonary infarction
72
Q

Clinical Features of Arterial Thrombi

A
  • rarer, more lethal than venous thrombi
  • limit oxygen rich blood to various organs (e.g. heart, brain, kidney) and cause tissue infarction
  • cell injury, inflammation
73
Q

Lines of Zahn

A

describe microscopic appearance of blood clots that form with alternating layers of pale platelets and darker red blood cells

  • presence = clot formed while under high blood pressure experiencing rapid flow (WHEN ALIVE)
  • usually areas ass. with heart and aorta
74
Q

Arterial System Thromboses (overview)

A

develop atop ruptured atherosclerotic plaques and rich in platlets

75
Q

Venous System Thromboses (overview)

A

form into long “casts” that grow toward heart and rich in RBCs
- MC in veins of lower extremeties (~90%)

76
Q

Superficial Vein Thromboses

A
  • ones in superficial veins rarely embolize (but may cause pain and edema and predispose skin to ulcers and infections
77
Q

Deep Veins with Thromboses

A 
= DVT; prone to embolization; less likely to have signs/symptoms and may only manifest after embolizes to lungs
Most likely to form in:
1. femoral vein
2. popliteal vein
3. iliac veins
78
Q

Disseminated Intravascular Coagulation (D.I.C.)

A

involves widespread microvascular coagulation; feature in many traumatic events

  • Activates widespread clotting and causes multiple organ systems to have ischemia/infarction–> lead to multi-system organ failure and death
  • Conversely–> may use all body’s clotting factors and platelets–> therefore inability to perform clotting and widespread hemorrage occurs
79
Q

What does Disseminated Intravascular Coagulation usually feature in?

A

Feature in many Traumatic Events:

  • crush injuries
  • motor vehicle accidents
  • obstetric complications
  • septic infections
  • advanced malignancy (cancer)
80
Q

What else is D.I.C. sometimes called?

A

“consumptive coagulopathy” b/c is may consume all body’s clotting potential and cause life-threatening clotting or hemorrhage

81
Q

Embolus

A

= unattached mass traveling through bloodstream; obstruct blood flow when reach vascular narrowing –> causes ischemic injury –> may cause tissue infarction
(Emboli = pleural term for embolus)

82
Q

Three kinds of Emboli

A
  1. solid emboli
  2. liquid emboli
  3. gaseous emboli
83
Q

Solid Emboli

A 
MC; originate form detached thrombi
Other Solid Emboli:
- fat globules
- cholesterol plaques
- fragments form metastatic cancers
- foreign materials traumatically implanted
84
Q

Liquid Emboli

A

include amniotic fluid –> a complication of birth and is “unpreventable, unpredictable” and often fatal

85
Q

Gaseous Emboli

A

involve atmospheric air injected via hypodermic needle, or nitrogen gas that bubbles out of blood during sudden decompression
- Caisson Disease

86
Q

Caisson Disease

A

aka Decompression sickness, the bends, or divers disease
- results from rapid decompression/ depressurization
- decompression allows dissolved gases (N) to form bubbles within blood
Symptoms: joint pain, headaches, dizziness, vertigo, visual abnormalities, seizures, loss of consciousness, itching skin, amnesia, muscle weakness/fatigue, dyspnea

87
Q

Caisson Disease most likely occurs from:

A
  1. rapidly ascending after deep-water diving
  2. emerging from a constructive caisson
  3. in aircraft that suddenly loses pressure
88
Q

Pulmonary Embolism (P.E.)

A

a consequence to DVT; ~90-95% originate from DVT
~80% Small and “clinically silent”
~2% Large
~ Medium

89
Q

Large P.E.s

A

may produce life-threatening vascular occlusion when become lodged in pulmonary arterial system

  • rare
  • saddle emboli
90
Q

Saddle Emboli

A

= when a large P.E. gets lodged in primary pulmonary artery bifurcation
- usually sudden death–> due to inducing a sustained arrhythmia OR by rupturing wall of right side of heart (massive hemorrhage)

91
Q

Medium Size P.E.s

A

when they obstruct pulmonary circulation…

Symptoms: dyspnea, cough, tachypnea, chest pain, systemic cyanosis, and pulmonary hypertension

92
Q

Pulmonary Hypertension

A

increase in BP with pulmonary arterial system; makes it difficult for blood to be pumped from right-side of heart through lungs
- Cor Pulmonale

93
Q

Cor pulmonale

A

enlargement (via hypertrophy) and failure of right-side of heart, following any pathology that causes pulmonary hypertension

94
Q

Systemic Thromboembolism

A

when a blood clot forms within systemic circulation (oxygen-rich arterial circulation)
- rarer compared to venous; but SERIOUS b/c can travel to any organ and cause infarction

95
Q

Main Cause of Systemic Thromoembolism

A

surviving myocardial infarction; ~80% originate post-myocardial infarction; 2/3 in left ventricle
- M.I. involves necrosis –> inflammation –> a abnormal cardiac conduction –> results in turbulent blood flow

96
Q

Risk Factors for Systemic Thromoembolism

A
  • dilation of left atrium of heart
  • cardiac vegetations (invective endocarditis–>mainly from bacteria)
  • aortic aneurysms
  • sites of atherosclerotic plaque formation
97
Q

What are the most common locations for a System Thromboembolism?

A

~75% in lower extremities,
~10% in CNS,
kidneys, intestines, or spleen

98
Q

Factors that predispose tissue to infarction due to a large systemic thromboembolism

A
  • absence of collateral blood supply

- tissue is highly vulnerable (CNS, heart, or kidneys)

99
Q

Anoxia

A

lack of oxygen within an organ

100
Q

Paradoxial Embolism

A

rare, but serious; when venous embolism passes through a cardiac defect and enters systemic (arterial) circulation
Represents ~2% of systemic emboli
- begins in venous system–> bypasses lungs–> and enters systemic (arterial) circulation
Due to:
- Ventricular Septal Defect (MC)
- Arterial Septal Defect

101
Q

Ventricular Septal Defect

A

most common cardiac defect that allows DVT to pass into arterial circulation

  • also MC congenital cardiac abnormality
  • “hole in the heart”
102
Q

Infarction

A

the process of developing an infarct; high morbidity and mortality

103
Q

infarct

A

area of necrosis that follows form significant occlusion of blood supply

104
Q

Many disabling or lethal conditions from infarctions

A
  • myocardial infarctions
  • cerebral infarctions
  • pulmonary infarctions
  • ischemic bowel disease (ischemic colitis)
  • gangrene
105
Q

Causes of Infarctions

A
  • arterial thromboemboli (cause vast majority)
  • tumors compressing a vessel, prolonged vasospasm, arterial dissection (tearing wall of artery), or twisting a vascular structure
106
Q

Morphological Patterns of Infarction

A
  • tend be to be wedged-shaped (triangular) with vascular occlusion at apex
    1. Red (hemorrhagic) infarcts
    2. white (anemic or pale) infarcts
107
Q

Severity of Infarction depends on:

A
  1. which tissue experiencing infarct
  2. how quickly blood supply is lost
  3. whether tissue naturally has a dual (collateral) blood supply
108
Q

Red Infarcts

A

involve blood accumulating within area of tissue death; develop in “loose tissues” where blood can collect/”pool” (like interstitium of lung); develop is tissues WITH DUAL blood supply

109
Q

White Infarcts

A

develop in “solid organs” or tissues with solid wall; develop in tissue with SINGLE blood supply
Ex: heart, kidneys, spleen

110
Q

Shock

A

is a process; systemic hypoperfusion of blood; in adequate blood supply to tissues, resulting in cellular injury, discomfort, and possible death
- life-threatening “circulatory failure”
Produces: decrease BP; highly lethal (mortality for all forms ~30%)

111
Q

Systemic Hypoperfuction

A

causes widespread injury to organs–> multi-organ failure (dysfunction or death)
-CNS, heart, kidneys, and liver, GI

112
Q

Two Categories of Shock

A
  1. Vasoconstrictive Shock

2. Vasodilation Shock

113
Q

Vasoconstrictive Shock

A

widespread SNS activation and vasocontriction; shunts blood from peripheral tissues to heart

114
Q

Features associated with Vasoconstrictive Shock

A
  • cool, “clammy”, cyanotic skin
  • increase in SNA will increase respiratory rate (tachycardia)
  • increase heart rate
  • hypotension + tachycardia = leads to rapid pulse ~ “thread pulse”
  • dyspnea, nausea, altered consciousness or syncope (fainting)
  • decrease urine output
115
Q

Two Types of Vasoconstrictive Shock

A
  1. Cardiogenic Shock

2. Hypovolemic Shock

116
Q

Cardiogenic Shock

A

(vascoconstrictive shock)
decrease hearts ability to pump blood, therefore decrease cardiac output
Causes:
- myocardial infarction
- sustained arrhythemia
- cardiac tamponade (fluid fills pericardial space)

117
Q

Hypovolemic Shock

A

(vasoconstrictive shock)
decrease cardiac output due to loss of blood or plasma volume; any sever hemorrhage >2% blood lost quickly can cause it
Causes:
- gunshot wounds, motor vehicle accidents, traumatic occupational injuries
- severe burn injuries–> severe plasma loss if >20% body covered by 3rd or 4th degree burns
- dehydration

118
Q

Vasodilatory Shock

A

“distributive shock” b/c blood “pools” (or distributes) in peripheral vessels
Causes: warm, “flushed” (erythematous) skin

119
Q

Three kinds of Vasodilatory Shock

A
  1. Septic Shock
  2. Neurogenic Shock
  3. Anaphylactic Shock
120
Q

Septic Shock

A

(Vasodilatory Shock)
develops from intense infection (septic inf.) and produces inflammatory immune rxn causing widespread vasodilation
Causes:
- MC =bacterial infections
- viral, fungal, and parasitic infections

121
Q

Severity of Septic Shock depends on:

A
  1. immune status of ind.
  2. virulence (harmfulness) of infective microbe
  3. presence of other co-morbid conditions ind. has
122
Q

Neurogenic Shock

A

develops following body’s inability to regulate vasoconstriction
- SNS controls autonomic vascular tone–> disruption of it causes severe vasodilation, hypotension, and brachycardia

123
Q

Causes of Neurogenic Shock

A

MC = acute spinal cord injury (spinal fractures, spinal cord hematomas)
- above T6 vert. level –> disrupts SNS outflow form thoracic sympathetic chain ganglia (T1-L2)–> results in unopposed vagal tone
More rare = following spinal anesthesia following adverse drug rxn (ADR)

124
Q

Anaphylactic Shock

A

serious allergic rxn (anaphylaxis); causes widespread swelling via vasodilation and breathing difficulties due to bronchoconstriction –> increases lethal risk
(Type I Hypersensitivity)

125
Q

Causes of Anaphylactic shock

A

an allergen; or exposure to latex, insect bites, various foods (shellfish or allergies), or following various ADRs

126
Q

Vasovagal Syncope

A

(neurocardiogenic syncope)
Triggers SNS: like site of blood, fear, injury, heat
Will: decrease HR and BP
- lightheaded, vision problems, “warm sensation”
First –> rule out serious cardiac pathology like EKG and “Echo”
Ex: Female Hysteria, Micturition Syncope

127
Q

Treatment for Vasodilatory Shock

A

elevate legs, increase fluid volume, vasoconstrictive meds (epipen)

128
Q

Treatment for Vasoconstrictive shock

A

defibrillation, CPR, minimize blood loss, lift legs, IV fluids

129
Q

Stages of Shock

A
  1. Nonprogressive shock
  2. Progessive Shock
  3. Irreversible Shock
130
Q

Nonprogressive Shock

A

earliest stage; SNS able to maintain profusion (cardiac output and blood pressure) to vital organs via compensatory mechanisms
Involves: tachycardia, peripheral vasoconstriction, and renal fluid conservation
- cool and “clammy” skin
**survival is possible –> if immediately corrected

131
Q

Progessive shock

A

progressively worsening organ system hypoperfusion and hypoxia
Causes: metabolic abnormalities in multiple organ systems –> switch aerobic metabolism to anaerobic metabolism
- rapid switch to glycolysis likely to produce metabolic lactic acidosis
**survival may be possible

132
Q

Irreversible Shock

A

severe multisystem tissue hypoxia and widespread membrane damage
**unable to correct = death!
Involves:
- failure of CNS, kidneys, and heart
- bowel infarctions –> lead intenstinal microflora into bloodstream = “bacteremic shock”

133
Q

Shock Index

A

= Heart rate divided by systolic blood pressure
Normal range –> 0.5 - 0.8 shock index
increase shock index; increase suspicion for shock

General Pathology -- Roecker (7 decks)

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