Pathophys

Question 1

Define natural history of disease

Answer 1

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

Question 2

Define lesion

Answer 2

tissue abnormality caused by disease or trauma

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

Question 3

Define sign

Answer 3

objective finding verified by the provider

can be documented

Question 4

Define symptom

Answer 4

subjective feeling or complaint from patient

Question 5

Define sequelae

Answer 5

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

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

Question 6

Define complication

Answer 6

new problem resulting from presence of disease

Question 7

Define inherited/familial disorders

Answer 7

mutations result in abnormal protein production

example: cystic fibrosis

Question 8

Define congenital disorders

Answer 8

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

example: atrial-septal defect

Question 9

Define metabolic disorders

Answer 9

Inherited or acquired deficiencies or abnormalities of metabolic systems or process

example: diabetes, phenylketonuria

Question 10

Define degenerative

Answer 10

Gradual breakdown of tissue or system and loss of function

Example: osteoarthritis, dementia

Question 11

Define neoplastic

Answer 11

Loss of growth control (tumor)

Example: cancer

Question 12

Define immunologic

Answer 12

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

Example: rheumatoid arthritis
poison ivy rash

Question 13

Define infectious disease

Answer 13

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

Example: influenza

Question 14

Define physical agent-induced

Answer 14

Trauma or toxicity due to physical agents

Example: burn

Question 15

Define nutritional disorders

Answer 15

Deficiency and excess of nutrients

Example: vitamin D deficiency, hypervitaminosis A

Question 16

Define iatrogenic

Answer 16

caused by health care system

example: errors, therapy, complication, misdiagnosis

Question 17

Define psychogenic

Answer 17

originating in the mind

Example: somatoform disorders

Question 18

Define idiopathic/primary disorders

Answer 18

causes are unknown

example: idiopathic scoliosis, primary hypertension

Question 19

Cell to cell communication occurs via

Answer 19

secreted molecules that interact and bind with complementary receptors

Question 20

Cell surface receptors are primary __ soluble hormones

Answer 20

water

example: insulin receptor

Question 21

Intracellular receptors are primary ___ soluble hormones

Answer 21

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

example: cortisol receptor

Question 22

What are the 4 types of cell-cell communication

Answer 22

autocrine

synaptic

paracrine

endocrine

Question 23

Describe autocrine communication

Answer 23

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

example: T lymphocytes, IL-2

Question 24

Describe synaptic communication

Answer 24

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

Example: neurotransmitters in synapse

Question 25

Describe paracrine communication

Answer 25

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

Question 26

Describe endocrine communication

Answer 26

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

Question 27

Define mitosis

Answer 27

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

Question 28

Define meiosis

Answer 28

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

Question 29

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

Answer 29

proliferation die via apoptosis differentiate to function tissue cells

Question 30

___ and ___ result from the balance between proliferation and apoptosis

Answer 30

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

Question 31

Define growth factors

Answer 31

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

Question 32

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

Answer 32

injury (reversible and irreversible - which leads to death)

Question 33

The response of cell to injury depends on

Answer 33

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

Question 34

Where is calcium most commonly found

Answer 34

extracellulary (1000x more than intracellular)

Question 35

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

Answer 35

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

Question 36

Increased intracellular calcium results in

Answer 36

biochemical changes water influx swelling loss of function of cell

Question 37

Define cori cycle

Answer 37

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

Question 38

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

Answer 38

decreases (enzymes are pH dependent) low pH denatures proteins causes morphologic changes

Question 39

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

Answer 39

decrease in oxidative phosphorylation in mitochondria increased anaerobic glycolysis, generating LA reduced intracellular pH, causing morphologic changes

Question 40

what do morphological changes reflect?

Answer 40

initial membrane damage

Question 41

morphologic changes due to Ca influx results in

Answer 41

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)

Question 42

critical biochemical events in irreversible cell injury

Answer 42

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)

Question 43

describe the two ways cells can die

Answer 43

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

Question 44

coagulative necrosis

Answer 44

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

Question 45

liquefactive necrosis

Answer 45

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

Question 46

caseous necrosis

Answer 46

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

Question 47

fat necrosis

Answer 47

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

Question 48

what are the 5 ways cells adapt

Answer 48

``` atrophy hypertrophy hyperplasia metaplasia dysplasia ```

Question 49

atrophy (physiologic and pathologic)

Answer 49

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

Question 50

hypertrophy (phys and path)

Answer 50

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)

Question 51

hyperplasia (path and phys)

Answer 51

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

Question 52

metaplasia

Answer 52

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)

Question 53

dysplasia

Answer 53

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

Question 54

3 stages of wound healing

Answer 54

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

Question 55

inflammatory phase of healing

Answer 55

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)

Question 56

proliferative phase of healing

Answer 56

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)

Question 57

remodeling phase of wound healing

Answer 57

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)

Question 58

healing by first intention

Answer 58

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

Question 59

healing by second intention

Answer 59

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)

Question 60

proud flesh

Answer 60

excessive granulation

Question 61

how does granulation occur

Answer 61

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

Question 62

what is fibrosis

Answer 62

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

Question 63

4 steps of scarring

Answer 63

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*

Question 64

what do metalloproteinases do

Answer 64

break down collagen | require the presence of Ca or zinc to work

Question 65

modifiers of wound remodeling

Answer 65

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

Question 66

tensile strength

Answer 66

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

Question 67

increased tensile strength is related to

Answer 67

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

Question 68

wound dehiscence

Answer 68

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

Question 69

hypertrophic scarring (keloid)

Answer 69

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

Question 70

wound contracture / remodeling

Answer 70

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!)