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Pathophysiology > Patho exam 1 > Flashcards

Patho exam 1 Flashcards

1
Q

Simple Squamous epithelium

A

location: lining of ventral cavities, blood vessels, alveoli of lungs
function: reduces friction, controls vessel permeability, secretion

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2
Q

Simple cubodial

A

location: glands and ducts
functions: secretion, absorption, limited protection

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3
Q

Simple columnar

A

location: lining of stomach, intestine, esophagus, gallbladder
functions: protection, secretion, and absorption

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4
Q

Transition epithelium

A

location: urinary bladder, renal pelvis of kidney, ureter

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5
Q

Pseduostratified columnar

A

location: lining of nasal passage, trachea, bronchi
function: protection and secretion

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6
Q

stratified squamous

A

location: skin, vagina, rectum, anus, mouth, throat
function: protection

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7
Q

Types of hypoxia

A
  • ischemia
  • hypoxemia
  • failure of oxidative phosphorylation
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8
Q

Ischeima

A
  • blood vessels and/or pumps do not work

- occlusion / pump failure

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9
Q

Hypoxemia

A
  • blood vessels and pumps work fine, but blood does not carry O2 properly
  • failure to perfuse or ventilate lungs, lack of RBC, low O2 in blood stream, inability of hemoglobin to bind/release O2
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10
Q

Failure of oxidative phosphorylation

A
  • cells are not using O2 properly

- cyanide, carbon monoxide

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11
Q

Patters of cell injury

A
  • hypoxia
  • poor nutrition
  • infections agents
  • chemical agents
  • physical agents
  • immune injury
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12
Q

Sources of intracelluar accumulations

A
  • triglycerides
  • glycogen
  • pigments
  • calcium
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13
Q

Dystrophic calcification

A
  • “wrong place”
  • calcium phosphate or calcium hydroxide create crystals which create masses
  • Normal: pinal glands, airway cartilages, mitral valve, aortic valve
  • abnormal: breast cancers, surgical scars, retained abortions
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14
Q

Metastatic calcifications

A
  • occur in abnormal places
  • high levels of calcium and/or phosphate
  • sites of pH gradients like small airways
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15
Q

Coagulation necrosis

A
  • usually due to ischemic hypoxia for free radical injury EXCEPT in the brain
  • death of groups of cells
  • DNA gets destroyed but cell membrane stays intact
  • replaced by scar, destroyed, walled off, or healed
  • has inflammatory response
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16
Q

Liquefactive necrosis

A
  • usually due to a bacterial infection
  • death of groups of cells
  • no inflammatory response
  • results from hydrolysis via lysosomal or WBC enzymes
  • cells disappear or leave gelatinous mass
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17
Q

Casous necrosis

A
  • also called saponification
  • usually due to immune injury
  • death of groups of cells
  • crumbled, gross-pale, cheesy
  • nucleus disappears, but the cells are not gone
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18
Q

Apoptosis

A
  • programmed cell death
  • single cell death
  • triggered by mitochondrial damage (leak caspase) or death receptors
  • usually due to immune response
  • cell membrane stays intact and remains are phagocytized by marcrophages
  • no inflammatory response
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19
Q

Dry gangrene

A
  • caused by coagulation necrosis
  • large scale death
  • no infection
20
Q

Wet gangrene

A
  • caused by liquefactive necrosis
  • large scale death
  • foul smelling
  • infected
21
Q

Gas gangrene

A
  • Clotridal gangrene

- flesh eating

22
Q

Atrophy

A
  • decrease in cell size not cell number
  • causes: loss of motor innervation, decreased blood supply, decreased hormonal stimulation, malnutrition
    ex: breast after pregnancy, loss of muscle mass in a cast
23
Q

Hypertrophy

A
  • increase in cell size not cell number
  • causes: increased work load, increased hormonal stimulation, normal stress like HTN
  • ex: muscle in weight lifters, heart in obese person, breast during pregnancy
24
Q

Hyperplaisa

A
  • increase in number of cells not size of cells
  • causes: compensatory, hormonal stimulation, genetic mutations
    ex. female breast during puberty, lymph nodes close to infection, t-cells during infection, bone marrow after giving blood
25
Q

Metaplasia

A
  • adaptive substitution of one cell type for another

- ex. pseudostratifed epithelium in airway changing to something more durable due to smoking

26
Q

Dysplasia

A
  • bad growth
  • atypical hyperplasia
  • loss of cell uniformity and orientation
  • resembles cancer, but is not invasive yet
  • results from genetic mutation to create a growth advantage
  • anaplasia is when it invades
27
Q

Roles of cells in inflammatory process

A
  • neutrophils: infections caused by common bacteria
  • lymphocytes: viral infections
  • plasma cells: spirochete disease (syphilis and lyme disease)
  • monocytes/macrophages: in TB and fungal infections
  • eosinophils: infections caused by worms
28
Q

Cardinal signs of acute inflammation

A
  • vasodilation: increased blood flow
  • neutorphil infiltration: margination, emigration, chemotaxis
  • increased capillary permeability: leakage of fluids and proteins
29
Q

Prostaglandins

A
  • inflammatory mediators
  • decrease vascular tone
  • increase pain
30
Q

Thromboxane A2

A
  • a prostaglandin
  • produced by platelets
  • vasocontriction and platelet aggregation
31
Q

Prostacyclin (PGI2)

A
  • a prostaglandin
  • produced by endothelial cells
  • vasodilation, prevents platelet aggreation
32
Q

Prostaglandin E2

A
  • a prostaglandin

- vasodilation, potentiates bradykinin, fever

33
Q

Leukotrines

A
  • inflammatory mediator
  • smooth muscle contraction
  • neutorphil chemotaxis
34
Q

Leukotriene C4

A
  • increases capillary permeability
  • breaks down to LTD4 and LTE4
  • causes smooth muscle contractions
35
Q

Leukotriene B4

A

-neutrophil and monocyte chemotaxis

36
Q

Define systemic inflammation

A
  • SIRS
  • systemic inflammatory response syndrome
  • large production of inflammatory mediators that results in multisystem organ failure
  • criteria (2 or more): temp >38 C or <36 C; HR >90bmp: RR >20/min: WBC >20,000 or <4, 000
37
Q

Transudate edema

A
  • salt water, little to no protein content leakage
  • results from alterations in starling forces and lymphatic failure
  • ex. heart failure, cirrhosis, liver failure
  • caused by: excess total body water, salt/fluid overloading, excess aldosterone, kidney failure, lymphatic obstructions, many vein issues
38
Q

Exudate edema

A
  • protein rich salt water
  • results from overly leaky capillaries
  • loose proteins
  • ex. inflammation, sepsis, burns
39
Q

Mechanisms of shock

A
  • hypovolemic shock
  • cardiogenic shock
  • distributive shock (warm)
  • obstructive shock
40
Q

Hypovolemic shock

A

-decrease in blood volume

41
Q

Cardiogenic shock

A

-pump failure

42
Q

Distributive shock

A

-profound vasodilation, lack of venous return

43
Q

Obstructive shock

A

-external compression of heart or its outflow

44
Q

Hypoxic injury mechanism

A
  • lack of O2 stops oxidative phosphorlylation and electron transport chain (edema is early sign as water rushes into cells)
  • anaerobic metabolism leads to lactic acid accumulation and pH drop
  • Ca+2 ATPase fails
  • Ca+2 entry is key step leading to cell death
45
Q

Gaucher’s disease

A

glucocerebroside

46
Q

Tay-Sachs’

A

ganglioside

Pathophysiology (5 decks)

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