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Derm EENT > Pathophys > Flashcards

Pathophys Flashcards

1
Q

Define natural history of disease

A

the progression of a disease process in an individual over time, in the absence of treatment

infection –> symptomatic –> immune response (5-7 days) –> bet better/die

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2
Q

Define lesion

A

tissue abnormality caused by disease or trauma

Examples: freckle, growth, tumor, plaque, diabetes (abnormality of organ function)

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3
Q

Define sign

A

objective finding verified by the provider

can be documented

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4
Q

Define symptom

A

subjective feeling or complaint from patient

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5
Q

Define sequelae

A

conditions resulting from disease or trauma
(consequence of previous disease)

Example: blindness after head injury, apraxia after a stroke, facial droop after cerebral hemorrhage

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6
Q

Define complication

A

new problem resulting from presence of disease

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7
Q

Define inherited/familial disorders

A

mutations result in abnormal protein production

example: cystic fibrosis

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8
Q

Define congenital disorders

A

prenatal (in utero) and neonatal (first two months) disorders of development

example: atrial-septal defect

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9
Q

Define metabolic disorders

A

Inherited or acquired deficiencies or abnormalities of metabolic systems or process

example: diabetes, phenylketonuria

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10
Q

Define degenerative

A

Gradual breakdown of tissue or system and loss of function

Example: osteoarthritis, dementia

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11
Q

Define neoplastic

A

Loss of growth control (tumor)

Example: cancer

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12
Q

Define immunologic

A

over or under responsive immune system against self antigens (autoimmune) and environmental antigens

Example: rheumatoid arthritis
poison ivy rash

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13
Q

Define infectious disease

A

Disease caused by microorganisms, parasites, or toxins resulting in tissue destruction

Example: influenza

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14
Q

Define physical agent-induced

A

Trauma or toxicity due to physical agents

Example: burn

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15
Q

Define nutritional disorders

A

Deficiency and excess of nutrients

Example: vitamin D deficiency, hypervitaminosis A

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16
Q

Define iatrogenic

A

caused by health care system

example: errors, therapy, complication, misdiagnosis

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17
Q

Define psychogenic

A

originating in the mind

Example: somatoform disorders

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18
Q

Define idiopathic/primary disorders

A

causes are unknown

example: idiopathic scoliosis, primary hypertension

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19
Q

Cell to cell communication occurs via

A

secreted molecules that interact and bind with complementary receptors

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20
Q

Cell surface receptors are primary __ soluble hormones

A

water

example: insulin receptor

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21
Q

Intracellular receptors are primary ___ soluble hormones

A

lipid (because they have to get through the plasma membrane)

example: cortisol receptor

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22
Q

What are the 4 types of cell-cell communication

A

autocrine

synaptic

paracrine

endocrine

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23
Q

Describe autocrine communication

A

cells detect, provide feedback to themselves and respond, rapid onset, short duration, very specific effect

example: T lymphocytes, IL-2

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24
Q

Describe synaptic communication

A

Nervous system, rapid onset, short duration, very specific effect

Example: neurotransmitters in synapse

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25
Q

Describe paracrine communication

A

chemicals secreted into local area then rapid destroy, only local cells affect, slight delay in action, intermediate duration, several actions

example: histamine, eicosanoids

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26
Q

Describe endocrine communication

A

Mediators which travel via bloodstream and target distant cells and tissues, delayed action, long duration, multiple significant actions (multiple tissues respond)
Most common with hormones, circulate throughout the body

Example: protein, steroid hormones

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27
Q

Define mitosis

A

somatic cell division where each daughter cell receives an identical and complete set of 46 chromosomes

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28
Q

Define meiosis

A

Gamete cell division in which the number of chromosomes is reduced in half (diploid to haploid, 23)

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29
Q

What are the possible outcomes for non-differentiated cells in tissues

A

proliferation

die via apoptosis

differentiate to function tissue cells

30
Q

___ and ___ result from the balance between proliferation and apoptosis

A

hyperplasia (enlargement due to proliferation of cells) and atrophy (cell becomes smaller)

*Note: hypertrophy is when the cell becomes larger, NOT the same as hyperplasia

31
Q

Define growth factors

A

Hormones secreted by cells which stimulates division and differentiation of themselves and other cells (capable of stimulating cellular growth, proliferation, healing, and cellular differentiation)

32
Q

What happens when a cell is unable to adapt to stress?

A

injury (reversible and irreversible - which leads to death)

33
Q

The response of cell to injury depends on

A

length of time of exposure (prolonged exposure = irreversible injury)
dose of injurious agent (large dose = cell death)
type of cell and its ability to adapt

34
Q

Where is calcium most commonly found

A

extracellulary (1000x more than intracellular)

35
Q

What enzymes does calcium activate when it accumulates in the cytosol and what do they do?

A

phospholipids destroy membrane phospholipids
proteases destroy proteins
ATPases result in ATP depletion
endonucleases degrade nuclear DNA

these will result in the plasma membrane and mitochondria to lose integrity

36
Q

Increased intracellular calcium results in

A

biochemical changes
water influx
swelling
loss of function of cell

37
Q

Define cori cycle

A

when the lactic acid produced during glycolysis moves to the liver to be made into glucose

38
Q

does lactic acid increase or decrease pH within a cell - what is the result of this

A

decreases (enzymes are pH dependent)

low pH denatures proteins
causes morphologic changes

39
Q

if there is a decrease or loss of ATP within a cell, what causes this? what will the decrease/loss cause?

A

decrease in oxidative phosphorylation in mitochondria

increased anaerobic glycolysis, generating LA
reduced intracellular pH, causing morphologic changes

40
Q

what do morphological changes reflect?

A

initial membrane damage

41
Q

morphologic changes due to Ca influx results in

A

increase in cell size (water influx)
swelling of mitochondria and ER (ATP decreases)
nuclear and chromosomal changes (decreased pH, enzyme activation)
detachment of ribosomes from ER (ATP depletion)
small cytoplasmic blebs (cytoskeleton disruption)

42
Q

critical biochemical events in irreversible cell injury

A

inability to reverse mitochondrial dysfunction (LA buildup and loss of ATP)
disturbances in plasma membrane function (membrane ion pump dysfunction - na, k, ca, water influx and cytoskeleton abnormalities)
oxygen radical injury (cell protein and lipid oxidation)

43
Q

describe the two ways cells can die

A

necrosis due to injury/unplanned events (pathological process) involves injury to MANY cells (release of lysosomal enzymes injure nearby cells and tissues), and initiates inflammatory response which may further injure surrounding cells

apoptosis due to planned/scheduled cell death (under specific physiologic and pathological circumstances), auto-destruction via cascade of enzymes, involves SINGLE cells (or small group), nucleus and chromatin changes, pronounced cytoplasmic blebbing with formation of membrane-bound apoptotic bodies (phagocytized by macrophages), non-inflammatory response

44
Q

coagulative necrosis

A

results from denaturation of proteins (example: ischemic death) due to low pH
tissue coagulates (does not disappear)
NO bacterial toxins or WBC being activated
blood supply is cut off and enzyme release is low

45
Q

liquefactive necrosis

A

results from autodigestion which dissolves cells (example: abscesses)
dump of lytic enzymes into tissues which activates all enzymes

46
Q

caseous necrosis

A

occurs with chronic and granulomatous inflammation
looks cheesy
TB MOST OF THE TIME

47
Q

fat necrosis

A

occurs when fat cells become necrotic - both liquefactive and coagulative necrosis occur
triglycerides cleaved and FFA are released, form aggregates of fat that macrophages remove resulting in misshape

48
Q

what are the 5 ways cells adapt

A 
atrophy
hypertrophy
hyperplasia
metaplasia
dysplasia
49
Q

atrophy (physiologic and pathologic)

A

shrinkage in cell size
intracellular components decrease
may progress to cell death via apoptosis if prolonged

phys - normal changes related to development or hormonal changes (embryo development, decreased workload, change in degree of endocrine stimulation, aging)

path - changes in cells and organs related to some pathology such as nerve damage, diminished blood supply, inadequate nutrition and/or loss of endocrine stimulation

50
Q

hypertrophy (phys and path)

A

increase in size of cell resulting in increase in organ size related to increased intracellular components (such as myofilaments)

phys - related to increased functional demand or specific hormonal stimulation, enhances function (example: muscle training)

path - related to increased functional demand or specific hormonal stimulation causing pathology resulting in altered function (example: acromegaly - growth hormone excess)

51
Q

hyperplasia (path and phys)

A

increase in the number of cells possibly resulting in increased volume (proliferation), requires DNA synthesis and only occurs in cells capable of proliferation, stimulated by growth factors, some cytokines and hormones

phys - caused by hormonal effects (endometrial hyperplasia during menstrual cycle), compensatory (wound healing)

path - increase in cellularity due to dysregulation of growth (driven by hormonal factors, increase in proliferation rate, increase in cellularity), may predispose to neoplasia

52
Q

metaplasia

A

reversible change in which one adult cell type is replaced by another adult cell type in order to function under stress or other pathologic stimulus (normal cells in wrong place)
usually caused by chronic irritation and inflammation
may predispose to neoplasia
may become dysplastic cells with continued exposure

Example: Barrett’s (squamous cells to columnar cells)

53
Q

dysplasia

A

deranged cell growth will cells of varied shape, size and appearance related to chronic irritation, inflammation, or other pathologic stimuli
loses morphological characteristics of mature differentiated cells
associated with genetic mutations (increased mutation rate = increased cancer risk)
*premalignant

54
Q

3 stages of wound healing

A
  1. inflammatory phase (up to 1 week)
  2. proliferation phase (days to weeks)
  3. remodeling phase (weeks to years)
55
Q

inflammatory phase of healing

A

suppress infection associated with injury then promote healing

  1. hemostasis stops bleeding and provides staging for cells to move through a fibrin matrix (stasis –> platelet aggregation –> thrombus formation)
  2. inflammation (vasodilation –> edema –> leukocyte diapedesis and phagocytosis)
56
Q

proliferative phase of healing

A
  1. granulation (growth of new tissue that is proliferating and growing into a place of deficit)
  2. contraction (wound edges begin to pull together via collagen contraction) - sign that collagen is being laid down, fibrin has no strength without collagen
  3. epitheliazation (epithelial cells grow over new granulation tissue) - anything over 3cm you need a skin graph!! (the longer this phase takes, the longer it takes for the matrix to form, the larger the scar will be)
57
Q

remodeling phase of wound healing

A
  1. reorganization of fibrotic tissue (fibers that don’t add to tensil strength are removed) and vasculature (collagen strands and blood vessels)
  2. further contraction (when MOST contraction occurs)
58
Q

healing by first intention

A

wound edges are approximated by sutures or other mechanisms to enhance healing rate and outcome

59
Q

healing by second intention

A

large tissue defect fills in slowly over time by gradual expansion of granulation tissue growing in from all margins in all directions (allow wound to heal on its own)
more intense inflammation = longer to heal
increased likelihood for significant scarring and wound contacture (granulation –> edge contraction –> scar formation)

60
Q

proud flesh

A

excessive granulation

61
Q

how does granulation occur

A

plasma protein deposition (protein matrix), fibroblast migration, collagen deposition, capillary ingrowth

62
Q

what is fibrosis

A

scaring
repair of damaged tissue requires replacement of parenchymal cells (functional part of organ) AND stromal proteins (structural proteins)

63
Q

4 steps of scarring

A
  1. fibroblast migration and proliferation
  2. collagen matrix deposition
  3. growth of new blood vessels (angiogensis)
  4. remodeling

first tissue is granulation tissue formed at base of wound

64
Q

what do metalloproteinases do

A

break down collagen

require the presence of Ca or zinc to work

65
Q

modifiers of wound remodeling

A 
nutrition
circulatory status
size, location, type of wound
metabolic status (diabetes decreases rate of wound healing)
glucocorticoids
infection
foreign bodies
early stress on wound
66
Q

tensile strength

A

tissues new max strength, increases slowly up to 80% of original strength, takes 3-12 months

67
Q

increased tensile strength is related to

A

net collagen deposition and collagen cross linking (Vit C facilitates collagen cross linking - think scurvy reopening because it could not remodel)

68
Q

wound dehiscence

A

opening of a previously closed wound caused by excessive stress or poor suture technique
usually occurs b/w 7-10 post operative
should be assumed that the defect involves the entire wound!
most common with abdominal surgery (laparotomy)
serosanguinous discharge is a sign

69
Q

hypertrophic scarring (keloid)

A 
raised scars due to excessive collagen deposition, excessive granulation tissue (delays re-epitheliazation)
genetic predisposition (esp with darker skin)
often hyperpigmented
70
Q

wound contracture / remodeling

A
  1. increased collagen and matrix deposition occurs as wound edges approach each other
  2. collagen cross linking
  3. contraction

the reaction is more exaggerated with healing by second intention (extensive scaring!)

Derm EENT (1 decks)

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