Inflammation II Flashcards

1
Q

What areas of the kidney are most susceptible to hypoxia and ischemia/ infarction?

A

Straight segment of the proximal tubule (medulla), thick ascending limb (medulla) (p.213)

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2
Q

What areas of the liver are most susceptible to hypoxia and ischemia/ infarction?

A

Area around the central vein (zone III) (p.213)

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3
Q

What areas of the colon are most susceptible to hypoxia and ischemia/ infarction?

A

Splenic flecture, rectum (p.213)

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4
Q

What is a watershed area?

A

An area receiving dual blood supply from the most distal branches of 2 arteries which protects these areas from single-vessel focal blockage. These areas are susceptible to ischemia from systemic hypoperfusion (p.213)

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5
Q

What regions of the brain are affected by hypoxic ischemic encephalopathy (HIE)?

A

The pyramidal cells of the hippocampus and Purkinje cells (p.213)

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6
Q

What is a ‘red infarct’?

A

A hemorrhagic infarct that occur in loose tissues with collaterals such as liver, lungs, or intestine, or following reperfusion (p.213)

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7
Q

What is a ‘pale’ infarct?

A

An infarct occuring in solid tissues with a single blood supply such as the heart, kidney, and spleen (p.213)

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8
Q

What causes a reperfusion injury?

A

Damage by free radicals (p.213)

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9
Q

What are the four characteristics of hypovolemic/ cardiogenic shock?

A

Low output failure; increased TPR; low cardiac output; cold, clammy patient (vasoconstriction) (p.214)

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10
Q

What are the four characteristics of septic shock?

A

High output failure; decreased TPR; dilated arterioles, high venous return; hot patient (vasodilation) (p.214)

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11
Q

What are six possible causes of atrophy?

A

1.) decreased hormones (uterus/vagina); 2.) decreased inervation (motor neuron damage); 3.) decreased blood flow; 4.) decreased nutrients; 5.) increased pressure (nephrolithiasis); 6.) occlusion of the secretory ducts (cystic fibrosis) (p.214)

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12
Q

Define atrophy.

A

Reduction in the number or the size of cells (p.214)

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13
Q

What are the five characteristics of inflammation?

A

Rubor, Dolor, Calor, Tumor (swelling), and loss of function (p.214)

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14
Q

Describe the vascular component of inflammation.

A

Increased vascular permeability, vasodilation, endothelial injury (p.214)

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15
Q

Describe the cellular component of inflammation.

A

Neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release (p.214)

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16
Q

Describe acute inflammation.

A

Rapid in onset (seconds to minutes) and lasts minutes to days (p.214)

17
Q

Describe chronic inflammation.

A

Characterized by persistent destruction and repair and associated with blood vessel proliferation and fibrosis (p.214)

18
Q

Which inflammatory mediators are responsible for acute inflammation?

A

Neutrophils, eosinophlis, and antibodies (p.214)

19
Q

Which inflammatory mediators are responsible for chronic inflammation?

A

Mononuclear cell mediated (p.214)

20
Q

What are the possible outcomes of acute inflammation?

A

Complete resolution, abcess formation, and progression to chronic inflammation (p.214)

21
Q

What are the possible outcomes of chronic inflammation?

A

Scarring and amyloidosis (p.214)

22
Q

What is a granuloma?

A

Nodular collection of epithelioid macrophages and giant cells (p.214)