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EOS P+P1 > Cellular Pathophysiology > Flashcards

Cellular Pathophysiology Flashcards

-Inflammation -anti-inflammatory drugs -Wound Healing

1
Q

What are the 5 cardinal signs of inflammation?

A 
Rubor: redness
Calor: warmth (heating)
Tumor: swelling
Dolor: pain
Functio laesa: loss of function
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2
Q

Cellular Adaptation: What is atrophy?

A

mass of functioning cells become reduced in size due to decrease in workload, blood supply, nutritional, hormonal + nervous stimulation, aging, disuse.

skeletal muscle, heart, secondary sex organs, brain
REVERSIBLE DAMAGE

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3
Q

Cellular Adaptation: What is hypertrophy?

A

increase in size of existing cells due to increased protein (nourishment).

physiological: increase growth of uterus and mammary glands in response to pregnancy, athetes

pathological: HTN resulting in increased force of heart contraction, over time causing the heart muscle to expand= CHF
REVERSIBLE DAMAGE

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4
Q

Cellular Adaptation: What is hyperplasia?

A

increase in number of cells within tissue.
physiological: hormonal stimulation = ductal cells in breast release estrogen= milk
pathological: excessive hormonal stimulation: BPH
REVERSIBLE DAMAGE

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5
Q

Cellular Adaptation: What is metaplasia?

A

one cell type replaced by another cell type. Cells sensitive to a stress are replaced by other cells which are more capable of withstanding to the adverse environment

eg. cilia in lungs of a smoker, GORD
REVERSIBLE DAMAGE

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6
Q

Cellular Adaptation: What is dysplasia?

A

abnormal cellular changes via shape, size and organisation of mature cells.

eg. epithelial tissue of the cervix and resp tract
IRREVERSIBLE - however if stimuli removed early enough can be reversible

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7
Q

Agents that contribute to cell injury?

A
  • hypoxia: hypoxemia, ischaemia (more common)
  • physical agents: temp, trauma, radiation, electick shock
  • chemicals and drugs
  • microbiological agents
  • immunologic reactions
  • genetic defects
  • nutritional imbalances
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8
Q

What is apoptosis?

A
  • programmed cellular death “cell suicide”
  • can be both physiological or pathological
  • effects one or a few cells
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9
Q

What is necrosis?

A
  • unplanned cellular death via autolysis (digest self)
  • only pathological response
  • affects many cells +/- tissue
  • contents of cells can be measured in blood and used for diagnosis (proteins=troponin=cardiac cell damage=MI)
  • types: coagulative, liquefactive, caseous, fat
  • types depend on tissue affected and injurious agent
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10
Q

What happens during the vascular phase of inflammation?

A
  • an agent causes damage to cells resulting in release of chemical mediatiors in local tissue which causes changes to blood vessels
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11
Q

What changes to blood vessels can the chemical mediators induce?

A
  • vasodilation of arterioles resulting in increased blood flow (hyperaemia) resulting in REDNESS + WARMTH
  • endothelial cells of capillary wall shrink increasing capillary permeability and allowing plasma to escape into intersititual fluid SWELLING and PAIN
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12
Q

What happens during the cellular phase of inflammation?

A

chemical mediators released from cell attract WBC (neutrophils + monocytes) to area of damage (chemotaxis).

  • Which helps remove or neutralise injurious agent
  • release further chemical mediators to recruite immune cells, potentiate inflam, initiate ealing
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13
Q

What are some chemical mediators of inflammation?

A

histamine: immediate vasodilator and increase permeablity to form exudate
chemotactic factors: attract neutrophils to site
cytokines: induce fever, chemotaxis, increase plasma protein
leukotrienes: bronchoconstriction, mucous production, increase vascular permeability, chemotaxis
bradykinin: vasodilator, increase permeablitiy, PAIN receptor (hyperalgesia), chemotaxis
PROSTAGLANDIN- cox 1 and 2 from mast cell membrane turn to arachodonic acd
cytoprotective PG1: increase gastric mucosa + platelet aggregation
inflam PG 2: further recruites WBC

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14
Q

What is chronic inflammation?

A
  • inflam lasting longer than 2 weeks as injurious agent has not been removed or neutralised
  • incomplete tissue repair
  • damage of functional cells (parenchymal) MI= replaced by fibrous tissue (scarring)= function compromised
  • granuloma formation- isolate injurious agents
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15
Q

NSAID cox-1 and cox-2 inhibitors are?

A

Aspirin (antiplatelet), Ibuprofen, paracetamol

anti inflam, anti-pyretic, analgesic

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16
Q

What is celecoxib MOA and adverse effects?

A

cox-2 inhibitor NSAID used to decrease inflam, antipyretic, anagelsic, PG in synovial fluid.
Adverse effect: increases platelet aggregation higher risk of cloting increase CV complications

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17
Q

What are hydrocortisone/cortisol and cortisone?

A

steroidal anti-inflammatory drugs that decrease PG production and pro-inflam transcription by inhibiting phospholipids transformation into arachidonic acid

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18
Q

What are leukotriene receptor antagonists/ montelukast?

A

drugs that inhibit the enzyme that produce leukotrienes. therefore decreasing inflam response. acute asthma

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19
Q

NSAID mechanism of action?

A

inhibit the synthesis of PGs via inhibiting the activity of the COX enzymes

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20
Q

Aspirins MOA and adverse effects are?

A

Inhibits both cox-1 + 2. Predominantly Cox-1 effect.
Reduces: inflam, pain, fever, decreases platelet aggregation (less likely to clot)
adverse: GIT integrity upset, consume after meal

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21
Q

MOA of corticosteriods

A
  • preventing synthesis of arachidonic acids (PG precursor)
  • inhibit gene expression and protein synthesis of majority of pro-inflam chemical mediators
  • reduction in syze of lymp nodes and spleen
  • inhibitition of helper t cells
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22
Q

Examples of corticosteriods and used for

A 
hydrocortisone, predisolone and dexamethasone used for anti inflammatory and immunosuppresive effects.
used for: Dermatitis
Rhinoritis
Asthma
Rheumatoid arthritis
Eczema
Ulcerative colitis
COPD
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23
Q

First intention wound healing is?

A

-minimal tissue loss, functional cell loss, scar formation

heals quick and uncomplicated

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24
Q

Second degree wound healing is?

A
  • significant tissue loss
  • major scar formation
  • extended healing time
  • little paraenchymal (functioning sell) regeneration
25
Q

Factors that affect wound healing include?

A
  • infection
  • movement of area
  • poor nutrient supply
  • poor o2 delivery
  • drug therapy
  • poor blood flow
26
Q

Stages of wound healing are..

A
  1. Firbin clot formation (fills initial gap, temporary seal from haemorrhage + infection, bringing wound edges together)
  2. Debridement (macrophages and neutrophils clean up debris and dead cells)
  3. Epithelialisation (tissue growth)
  4. Regeneration phase
  5. Remodelling/ Maturation phase
27
Q

Regeneration phase of wound healing includes

A

granulation connective tissue grows into wound consisting of:

  • collagen fibers (protein used for strength and structure
  • capillaries: deliver nutrients, cells and cofactors
  • lymphatic vessels: drain excess fluid/ wound exudate
  • fibroblasts: make and eposit collagen
  • myofibroblasts- drain wound together
  • macrophages: remove further debris,
28
Q

Remodelling/ maturation phase includes

A
  • 2 week post injury
  • scar tissue remodelling and becomes avascular
  • collagen fibres create extra strength
29
Q

What is bacteria?

A
  • prokaryotes (no nucleus)
  • alive
  • dna double standed
    -peptoglycon cell wall
  • asexual: divide via binary fusion
    coccus, bacilius, staph, strep
30
Q

What are viruses?

A
  • not alive
  • have either dna or rna
  • protein coat membrane
  • interceullular parasites
    HIV hep c
31
Q

what is the chain of infection?

A
  1. organism (pathogenic microbe)
  2. reservoir
  3. portal of exit (how it leaves: blood, vomit, aerosol, urine)
  4. transmission (indirect or direct)
  5. portal of entry
  6. vulnerale hosts (immunisations, good nutrition)
32
Q

Difference between prokaryotic and eukaryotic cells?

A

Prokayrotic dna different, do not have true nucleas, no membrane bound organelles, different types of ribosomes, have a cell wall.

33
Q

Methods for categorising bacteria are?

A

Histological stain (+ or -), shape (coccus/bacillus), arrangement (staph irreg/strep chains), metabolism type (aerobic/anaerobic).

34
Q

What are some characteristics of gram + bacteria?

A
  • 3 x layered cell wall (plasma membrane, cell wall, capsule)
  • thick peptidoglycan cell wall
  • purple stane
  • more easily treatable with ABs
35
Q

Characteristics of gram - cells

A
  • thin peptidoglycan cell wall
  • another layer of plasma membrane (4)
  • red gram stain
  • harder to treat
36
Q

What is an exotoxin?

A

toxin produced by bacteria, most commonly gram postive. Proteins unstable over 60 degrees and highly toxic to human cells

37
Q

What is an endotoxin?

A
  • present in cell wall of gram negative bacteria only
  • released on death of bacterium
  • heat tolerant
  • can cause fever and shock
38
Q

What does bactericidal mean and what is an example?

A
  • AB that kills the bacteria eg. penicilin
39
Q

What does bacteriostatic mean and what is an example?

A
  • drug that decreases rate of reproduction by inhibiting growth and replication. Aiding immune system to destroy. Tetracylin
40
Q

What is broad and narrow spectrum?

A

broad ABs are effective against both gram postive and negative organisms. narrow only effective against one or the other

41
Q

What is aminoglycosides effected bacteria, eg and MOA?

A

effects gram negative via inhibiting protein synthesis 30s. eg. straptomycin, gentamicin

42
Q

What is cephalosporins effected bacteria, eg and MOA?

A

Both gram postive and negative via inhibiting cell wall synthesis. Cepahlothein

43
Q

What is penicillin effected bacteria, eg and MOA?

A

Gram positive via cell wall synthesis. penicilin G

44
Q

What is tetrocyclins effected bacteria, eg and MOA?

A

both positive and negative via protein synthesis of 30s. eg. tetracyclin BACTERIOSTATIC

45
Q

What is quinolones effected bacteria, eg and MOA?

A

Both grams via inhibiting DNA replication. Ciproflaxin

46
Q

What is macrolides effected bacteria, eg and MOA?

A

Gram positive by inhibiting protein synthesis of 50s sub unit. erythomycin

47
Q

What is sulfonemides effected bacteria, eg and MOA?

A

both grams via inhibiting folate synthesis. sulfamethoxazole

48
Q

What is glycoproteins effected bacteria, eg and MOA?

A

Gram positive via cell wall synthesis. Vancomycin

49
Q

MOA cell wall inhibitors

A

abscence of peptidoglycan call wall results in osmosis and cell bursting. amoxycilin, cephalosporins, penicilins, vancomycins

50
Q

MOA protein synthesis inhibitors

A

acting on ribosomes preventing bacteria making new protiens resulting in inhibition of cell growth and replication. eythromycin, gentamicin, tetraclyines, glyclicines

51
Q

MOA DNA synthesis inhibitors

A

DNA synthesis vital for bacterial cell replication and reproduction. quinlones and rifampin

52
Q

MOA bacterial folic acid synthesis

A

folic acid required to produce ATP. ABS interfere with synthesis sulfamethoxable, trimethoprime

53
Q

Mechanism of antiobitioc resistance

A

reproduce asexually, mutating. Resistance is passed on via its genes

54
Q

The mechanisms bacteria use to counteract antibiotics are:

A

Actively removing the antibiotic from its cell
Producing enzymes that inactivate the antibiotic
Using different metabolic pathways to those being inhibited by the antibiotic
Altering the binding site that antibiotics usually adhere to.

55
Q

Stages of infection

A
  1. Incubation period (organism enters)
  2. Prodromal period (signs and symptoms)
  3. Acute period (infectious disease development)
  4. total recover
  5. chronic infection with mild signs
56
Q

S+S of infection local

A

-pain, swelling, redness warmth (local signs of inflammation)

57
Q

S+S infection systemic

A

fever, fatigue, headache, nausea

58
Q

What is the innate imunity and the components?

A

non specific immediate protection against pathogens. Same reaction regardless of the invador.
1st line defense:
external protection- skin, mucous membrane (mechanical); sweat, pH, sebaceous oil glands (chemical)
2nd line defense:
-chemicals
- cells (phagocytes, basophils, mast cells- chemical release)
- inflammation and temperature

59
Q

Cells within the innate immunity system?

A

NK cells- apoptotic effect on pathogens

Phagocytes - neutrophils, monocytes/macrophages

EOS P+P1 (1 decks)

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