more path Flashcards

1
Q

shock definition

A

Cardiovascular collapse, resulting in systemic hypoperfusion caused by reduction either in cardiac output or effective circulating blood volume
* Results in hypotension, followed by impaired tissue perfusion and cellular hypoxia
* Persistence of shock eventually causes irreversible tissue injury> death

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2
Q

Hypovolemic Shock

A

Results from loss of blood or plasma volume
* Hemorrhage
* Fluid loss from severe burns or trauma
* Dehydration

Compensatory: increase HR, vasoconstriction > BP and BV rises

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3
Q

Cardiogenic Shock

A

Results from myocardial pump failure
* Intrinsic myocardial damage: infarction
* Ventricular arrhythmias
* Extrinsic compression: cardiac tamponade (fluid in pericardium)
* Outflow obstruction: pulmonary embolism

In all cases, diminution of systolic volume and cardiac output
Causes: DIC, metabolic acidosis

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4
Q

neurogenic shock

A

Loss of sympathetic tone and thus unopposed parasympathetic response driven by the vagus nerve.
Consequently, patients suffer from instability in blood pressure, heart rate, and temperature regulation
Results from vasomotor paralysis (autonomic nervous system)> loss of vascular tone + peripheral pooling of blood
* Spinal cord injury
* Anesthetic accident
* Encephalitis
* Excruciating pain (colic in horses, Gastric Dilation and Volvulus in dogs)

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5
Q

Anaphylactic (allergic) Shock

A
  1. Results from generalized IgE-mediated type 1 hypersensitivity response
  2. systemic vasodilation + ^ vascular permeability
  3. sudden ^ in vascular bed capacitance
  4. hypotension + tissue hypoperfusion + cellular anoxia
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6
Q

Septic shock

A

Results from spread and expansion of an initially localized infection (e.g., abscess, peritonitis, pneumonia) into bloodstream
^ incidence: improved life support for high-risk patients, ^ use of invasive procedures, ^ numbers of immunocompromised hosts
Causes:
* Endotoxin-producing Gram-negative bacilli: endotoxic shock
* Endotoxins: bacterial wall lipopolysaccharides (LPS) that are released when cell walls are degraded in an inflammatory response
* Analogous molecules in walls of Gram-positive bacteria and fungi can also elicit septic shock

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7
Q

Septic shock pathogenesis

A
  1. Free LPS attaches to a circulating LPS-binding protein
  2. complex binds to CD14
  3. complex binds to TLR-4
  4. TLR-4 signal transduction
  5. activates vascular wall cells and leukocytes + initiates a cascade of cytokine mediators

TLR-4 on endothelial cells
Down-regulation of natural anticoagulation mechanisms: decrease synthesis of tissue factor pathway inhibitor (TFPI) and thrombomodulin
TLR-4 on monocytes and macrophages
Profound mononuclear cell activation > primarily production of IL-1 and TNF > ultimate effect depends on LPS doses

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8
Q

Low dose LPS effecr

A

Produce TNF and IL-1 at levels with local effects
Act on endothelial cells to stimulate expression of adhesion molecules > enhance acute inflammatory response > eliminate bacteria
Activate complement > local bacterial eradication

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9
Q

LPS effect moderate dose

A

Produce TNF and IL-1 at levels with local and systemic effects
Systemic effects: fever, ^ synthesis of acute phase reactants
Produce secondary cytokines: NO
diminished endothelial cell production of thrombomodulin and TFPI > pro-thrombotic effect

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10
Q

High dose LPS effect

A

septic shock occurs
Due to massive systemic effect of TNF, IL-1, and secondary cytokines
* Systemic vasodilation (hypotension)
* Diminished myocardial contractility
* Widespread endothelial injury and activation > systemic leukocyte adhesion + pulmonary alveolar capillary damage (ARDS/DAD)
* Activation of coagulation system > DIC

Multiorgan failure and death: due to combined effects of widespread vasodilation, myocardial pump failure, and DIC

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11
Q

High dose LPS effect

A

septic shock occurs
Due to massive systemic effect of TNF, IL-1, and secondary cytokines
* Systemic vasodilation (hypotension)
* Diminished myocardial contractility
* Widespread endothelial injury and activation > systemic leukocyte adhesion + pulmonary alveolar capillary damage (ARDS/DAD)
* Activation of coagulation system > DIC

Multiorgan failure and death: due to combined effects of widespread vasodilation, myocardial pump failure, and DIC

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12
Q

Initial Non-Progressive Phase of shock

A

Involves activation of reflex compensatory mechanisms that maintain perfusion of organs
Compensatory mechanism are neurohormonal
* Baroreceptor reflexes
* Release of catecholamines
* Activation of renin-angiotensin axis
* Antidiuretic hormone release
* Generalized sympathetic stimulation

Effects
* Tachycardia
* Peripheral vasoconstriction
* Renal conservation of fluid

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13
Q

Progressive stage of shock

A

Involves onset of tissue hypoperfusion and worsening circulatory and metabolic imbalances (including acidosis) > organs begin to fail
However, damage is reversible if initiating insult corrected
Effects
1. Widespread tissue **hypoxia **
2. ^ anaerobic glycolysis
3. production of **lactic acidosis **
5. decrease tissue pH
6. blunts vasomotor response
7. Arteriolar dilation > **blood pools in microcirculation **
* decrease cardiac output
* Anoxic injury to endothelial cells > DIC

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14
Q

Irreversible stage of shock

A

Involves onset of irreversible organ failure due to tissue hypoperfusion
Effects: widespread irreversible cell injury
* Lysosomal enzyme leakage > further cell death
* NO synthesis > decrease myocardial contractile function
* Acute tubular necrosis > renal failure

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15
Q

Stages of shock

A
  1. Initial non progressive
  2. progressive
  3. irreversible

KNOW THIS GRAPH!!!

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16
Q

Fibrosis

A

The repair of damaged tissue by replacement with connective tissue (collagen)
5 components
* Inflammation
* Angiogenesis
* Fibroblast migration and proliferation
* Scar formation
* Connective tissue remodeling

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17
Q

Fibrosis

A

The repair of damaged tissue by replacement with connective tissue (collagen)
5 components
* Inflammation
* Angiogenesis
* Fibroblast migration and proliferation
* Scar formation
* Connective tissue remodeling

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18
Q

angiogenesis

A

Formation of new blood vessels
2 mechanisms:
* Angiogenesis from pre-existing vessels (Primary mechanism)
* Angiogenesis from endothelial precursor cells (EPC migrate from bone marrow to site of injury and differentiated into mature blood vessels)

New vessels (capillary buds) are leaky and the tissue around them is edematous

Angiogenesis = important in fibrosis AND tumor growth

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19
Q

Vascular Endothelial Growth Factor (VEGF)

A

Stimulates endothelial cells to:
* Survive
* Proliferate
* Mobilize

20
Q

Healing by first intention

A

Clean (uninfected), sutured, surgical incision
Within 24 hours
1. Hemostasis: the wound is immediately filled with clotted blood containing fibrin
2. Neutrophils appear at edge of incision
3. Epidermis at edge of wounds thickens due to mitotic activity of basal cells
4. Epithelial cells begin to migrate from the wound edge toward the center

By day 3:
* Neutrophils replaced by macrophages
* Formation of granulation tissue (Angiogenesis + fibroblast proliferation)
* Epithelial proliferation continues

By day 5:
* Incision filled with granulation tissue
* Collagen fibrils begin to bridge incision
* Epidermis returns to normal thickness

Second week to months later:
* Leukocytes, edema, and increased vascularity disappear
* Granulation tissue replaced by scar
* Increased deposition and remodeling of collagen
* Wound strength increases but never reaches original tissue tensile strength

21
Q

Wound strength after first intention

A

Suture removal (~10 days): Strength is 10% of intact skin

Increases and reaches 70 to 80% after three months (plateau)
Never fully regains strength of normal skin

22
Q

Healing by second intention differences from first intention

A

Larger defect than first intention (excisional wound, ulcer, ruptured abscess)
More intense inflammatory reaction
More granulation tissue → bigger scar
Wound is closed by wound contraction
Due to action of MYOFIBROBLASTS (contractile)

23
Q

local and systemic factors that impair wound healing

A

Systemic: Nutrition:
* Protein deficiency (malnutrition, cachexia)
* Vit C deficiency (Inhibits collagen synthesis = scurvy)
* Metabolic disease (Diabetes mellitus)

Local factors:
* Infection =most important
* Foreign bodies

24
Q

Pathologic wound healing

A

Excessive formation of the repair components
* Hypertrophic scar: Proud flesh – exuberant granulation tissue

Contracture
* Excessive contraction in size of the wound
* Common after serious burns
* Can compromise joint movement

25
Q

Amyloidosis

A

Amyloidosis is not a specific disease, but is a group of diseases characterized by the deposition of amyloid.

either a generalized, systemic disease leading to multiorgan dysfunction or it can be a localized disease

Pathogenesis:
Abnormal folding of proteins → insoluble fibrils deposit in extracellular tissue → protein deposits interfere with normal cellular function

26
Q

Amyloid

A

Pathologic proteinaceous substance, deposited in the extracellular space in various tissues and organs
Beta-pleated sheet arrangement

27
Q

3 most common forms of amyloid

A
  1. AL (amyloid light chain)
    Derived from plasma cells; immunoglobulin light chains
  2. AA (amyloid associated)
    Derived from serum amyloid A protein made in the liver (remember - acute phase protein!)

  3. Found in Alzheimer’s plaques and old dogs
28
Q

Primary amyloidosis

A

Plasma cell tumors/multiple myeloma
AL (light chain) amyloid

29
Q

Secondary/reactive amyloidosis

A

Persistent inflammation – e.g tuberculosis, osteomyelitis
AA amyloid

30
Q

Benign neoplasia

A
  • Non-invasive
  • Does not metastasize
  • Local surgical removal is usually curative

Named for the tissue of origin with the addition of the suffix “oma”
* Mesenchymal tumors typically follow this rule
* Benign tumor of adipose: Lipo + oma
* Benign tumor of fibroblasts: Fibro + oma
* Benign tumor of bone: Osteo + oma

31
Q

adenoma

A

benign tumor derived from glandular tissue

32
Q

malignant tumors

A
  • Locally invasive and destructive growth
  • Can/Will metastasize
33
Q

sarcoma

A

malignant Neoplasms derived from mesenchymal (connective tissue) elements

34
Q

carcinoma

A

Malignant neoplasms derived from epithelial cell origin

35
Q

differentiation

A

he extent to which neoplastic cells resemble the normal population of cells they were derived from
* benign neoplasms - generally well-differentiated
* malignant neoplasms - well to poorly differentiated

35
Q

differentiation

A

he extent to which neoplastic cells resemble the normal population of cells they were derived from
* benign neoplasms - generally well-differentiated
* malignant neoplasms - well to poorly differentiated

36
Q

anaplastic

A

tumor is usually malignant
means poorly differentiated

37
Q

Morphologic characteristics used to evaluate differentiation

A

cellular pleomorphism
* **Variation in size and shape-anisocytosis **

nuclear morphology-anisokaryosis
nuclear/cytoplasmic ratio (N:C): higher = malignant
mitoses-type: more mitosis= bad, atypical= bad
cellular orientation: loss of polarity=bad

38
Q

Functional differentiation

A

do tumor cells behave like the tissue from which they arise
* benign neoplastic cells are more likely to function like their normal non-neoplastic counterparts than malignant cells are

39
Q

local invasiveness

A

Benign neoplasms tend to grow slowly and may elicit capsule formation
Malignancies grow by invasion and destruction of adjacent tissue
Local invasiveness is one of the most important characteristic of malignancies
* an evaluation of ‘surgical margins’ will allow evaluation of invasiveness
* if you don’t completely resect around a malignancy, it is more likely to recur

40
Q

neoplasms metastasize by:

A
  • blood stream (hematogenous spread) (sarcomas)
  • lymphatic channels and nodes (carcinomas)
  • direct implantation in body cavities and on surfaces by contact (carcinomatosis)
41
Q

hyperplasia

A

Non neoplastic
increased number of cells in a tissue
Orderly pattern of growth
Cells resemble normal cells
May see increased mitotic figures
Can be normal (Hormonal or compensatory)
Can be responsive (Excess hormones or chronic irritation)

42
Q

dysplasia

A

the disorderly but NON-NEOPLASTIC growth of epithelial cells
* Cells show a loss of uniformity-pleomorphism
* May see increased mitotic figures

May progress to neoplasia
* Carcinoma in situ-when dysplastic changes are full thickness but do notpenetrate the basement membrane
* Invasive carcinoma

43
Q

Carcinoma in situ

A

when dysplastic changes are full thickness but do not
penetrate the basement membrane

44
Q

metaplasia

A

replacement of one adult cell type by another of the same germ line
* Often associated with prolonged tissue damage and repair
* May be reversible if source of irritation is removed
* Or may be pre-neoplastic