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2002MSC Pathophysiology > Quiz 1 - Module 1 > Flashcards

Quiz 1 - Module 1 Flashcards

1
Q

Which of the following cells do not normally circulate in the blood?

Neutrophils
Monocytes
Eosinophils
Mast cells

A

Mast cells

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2
Q

An increase in cell size resulting in an increase in the size of the organ is an example of?

Hyperplasia
Atrophy
Hypertrophy
Apoptosis

A

Hypertrophy

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3
Q

Which of these is a physiological hyperplasia

Skin warts
excesssive endometrial hyperplasia
englarged prostate
liver regeneration

A

liver regeneration

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4
Q

Identify the leading causes of mortality inter- /nationally, and diseases affecting First Nations and non-Indigenous Australians

A 
Coronary Heart Disease
Cancer
HIV/AIDS
Respiratory conditions 
** these are all preventable by lifestyle changes 
Stroke 
RHD
DM
CKD
IHD
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5
Q

Provide examples of ways in which cells detect and adapt to stress

A

If a cells stable ‘homeostasis’ environment becomes stressed it results in ‘adaption’ - reversible changes in structure / function = survival

  • Hypertrophy, hyperplasia, atrophy, metaplasia

If stress is too great it can lead to cell injury. Irreversible stress causes cell death by 3 mechanisms
- Apoptosis (programmed), necrosis (mortification/death), autophagy (eat oneself)

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6
Q

What are the two cellular responses to stress

A

Acute = physiological

Chronic/severe = pathological

Chronic /severe stress cause cell death = apoptosis or necrosis

Necrosis = reversible/irreversible, leading to cell swelling / cell damage + then inflammation

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7
Q

Provide examples of physiological/pathological adaptation

A

Physiologic : Hyperplasia

  • Hormonal - when needed (breast tissue, puberty, pregnancy)
  • compensatory - damage / resection (liver regeneration

Pathologic : Hyperplasia

  • excess hormone / growth factors (abnormal menstural bleeding, viral infections, benign prostatic hyperplasia (excess androgen)
  • Mechanisms - growth factors stimulate cell signalling resulting in cellular proliferation
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8
Q

Describe how nuclei and proteins are identified in microscopic slides (histology)

A

By metaplasia : transformation of one cell type to another

e.g. columnar to squamous epithelium

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9
Q

Compare the histologic presentation of necrosis and apoptosis

A

Cell damage = necrosis

During initial stages of ischemia, lack of O2 leads to ATP depletion, itnracellular Na+ accumulation causes osmotic cell swelling (reversible), before memrbane rupture

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10
Q

Describe types of necrosis

Coagulative

A

Coagulative Necrosis

  • Caused by coagulation causing ischemia
    • tissue swelling, loss of nuclei
    • infarct is firm to touch, blocks proteolysis (denaturation of proteins + enzymes)
    • all organ by brain
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11
Q

What are the four types of necrosis

A

Coagulative
Liquifactive
Caseous
Gangrenous

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12
Q

Describe types of necrosis

Liquifactive

A

Hypoxia (brain)
Bacterial
Fungal infections
Digestion of dead cells

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13
Q

Describe types of necrosis

Gangrenous

A

Affects peripheral limbs, lack of oxygen, diabetes, PAD

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14
Q

Describe types of necrosis

Caseous

A

typical in tuberculosis, inflammation, dead cells, infiltrated leukocytes

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15
Q

What are the mechanisms of cell injury / death

A

Mitochondrial damage (leakage of pro-apoptotic proteins)

Decreased ATP (multiple downstream effects)

Entry of Ca2+, increased ROS (damage to lipids, proteins, DNA), protein misfolding and DNA damage

Membrane damage (loss of cellular components, enzyme digestion of cellular components)

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16
Q

Understand specific pathways/ molecules involved in apoptosis

A

‘Programmed cell death’
- stimulated by toxins, ischemia, radiation

Physiological Apoptosis

  • embryogenesis - death of specific cell type at defined time during development
  • cell loss in proliferating cell populations - immature lypmphocytes in bone marrow

Pathologic apoptosis

  • DNA damage - radiation, cytoxic anticancer drugs
  • accumulation of misfolded proteins - DNA mutation, coding for proteins (neuro-degerative disorders)
  • cell death in certain disorders (HIV, Hepatitis)
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17
Q

Describe morphological and biochemical changes within cells during apoptosis

A

Morphological
- cell shrinkage
chromatin condesnation (DNA condense)
- membrane blebbing, small cell fragments containing organelles
- phagocytosis of apoptotic bodies by macrophages

Biochemical

  • DNA and protein breakdown
  • Membrane alterations, phagocytosis
    • outer cell membrane recognised by phagocyte receptors
    • experimentally revealed using the annexin V antibody
18
Q

What is necrosis

A

Permeation of cell membrane

Inflammatory response

19
Q

What is apoptosis

A

Programmed cell death
- DNA damage
No inflammatory response

20
Q

What stresses are mitochondrial sensitive to?

A

Increased calcium
ROS
Decreased O2
Toxins

21
Q

What are antioxidants?

A

Simple molecules that block or inactivate free radicals

- Vitamin A, C, E, glutathione, bilirubin

22
Q

Name 2 clinical examples of cell damage and what occurs

A

Ischemia and Hypoxaemic injury

  • ischemia decreased O2 delivery to tissues from arterial blockage
  • decreased venous drainage; decreased arterial inflow causing ischemia
  • hypoxia decreased oxygen in blood
  • primary cause of cell deaht -> ATP depletion
23
Q

Name 2 clinical examples of cell damage

A

Ischemia / reperfusion

Chemical / toxin injury

24
Q

Define ischaemia / reperfusion

A
  • Restoration of blood flow futher exacerbates injury
  • causes new and distinct damaging processes (decreased O2)
    - increased ROS from mitochondrial damage
    - inflammation caused by macrophages
25
Define chemical/ toxin injury
- prescribed drugs, pollutants, food born toxins - target liver - 2 major mechanisms 1. direct cell injury 2. secondary metabolism - drugs metabolised, products are toxic / deplete cells of nutrients
26
Describe the mechanisms of apoptosis
- too much apoptosis = neurodegeneration - too little apoptosis = cancer - initiation - activation of caspases by - instrinsic pathway (mitochondrial) - extrinsic pathway (death receptor) - execution - degradation of cell components
27
What is autophagic cell death?
Autophagy = eat oneself - self digestion of cells during starvation - merge with lysosoem = eventual cell death = NS + muscular diseases
28
What happens when apoptosis increases/ deacreases?
Increased apoptosis (protein accumulation) = neurodegeneration = decreased (p53 mutation) = cancer
29
Describe the different intracellular accumulations that resilt in cell death?
2 types - normal cellular constituents (water, lipids, proteins) - abnormal substances, ifnectious agents, abnormal synthesis/metabolism
30
What are the 4 main causes of accumulations?
1. Abnormal metabolism 2. Defect in protein folding, transport 3. Lack of enzyme 4. Ingestion of indigestable materials
31
Describe steatosis?
accumulation of triglycerides - liver, msucle, heart, kidneys, Aetiology - toxins (alcohol), protein malnutrition, diabetes, obesity - causes - lipid accumulation (excess alcohol), decreased metabolism (hypoxia), cell death, inflammation = organ failure = cancer
32
What is inflammation?
- biological responses aimed at destroying invading pathogens / eliminating damaged cells - w/o wounds wouldn't heal, infectious would overwhelm homeostasis - dysregulations = chronic diseases - composed of blood vessels + leukocytes
33
What is the difference between acute vs chronic inflammation?
Acute - minutes, hours, days - leukocytes (neutrophil), infiltration, oedema Chronic - can follow acute, lasts for months - infiltration of macrophages, lymphocytes, causes fibrosis, tissue destruction
34
What are clinical manifestations?
- vasodilation - histamine (rubor) - heat (calor) - dilation of artioles + capillary beds - icnreased vascular permeability (venules) - oedema (tumour; oncotic pressure) - local pain (dolar) induced by prostaglandin, cytokine release
35
What is the blood vessel involvement in inflammation?
acute inflammation delivers leukocytes to area of infection - increased erythema, calor - extravation + deposition of plasma fluid + proteins - emigration / accumulation of leukocytes
36
What are some stimulis for inflammation?
Infectious material - bacterial, viruses, parasitic - recognised by leukocytes - stimulates inflammatory mediators Tissue necrosis - MI, trauma, hypoxia - releases cell contents ``` Foreign bodies (splinters) - introduce microbes, cause cell necrosis ```
37
What are the two blood vessel reactions - acute inflammation
Transudate - movement of fluid exept proteins, no cellular material, low specific gravity into interstitial space Exudate - escape of fluids / proteins, cellular debris, high specific gravity from blood --> IF (inflammation) * **both can cause oedema * ** Pus = purlent exudate = leukocytes, microbes, debris
38
What does flow and calibre mean (blood vessel reactions)
Vasodilation - early, caused by histamine _ nitric oxide release e.g. transient ischemia - Also causes increased permeability of microvasuclature - decreased red blood flow, increased viscosity, congestion - encourages leukocytes to accumulate upon endothelium, migrate from circulation into tissue
39
Describe vascular permeability
``` A. Normal B. Retraction of endotheilial cells C. Endothelial injury D. Leukocute mediated cascilar injury E. Icnreased transcytosis ```
40
Describe the role of leukocytes and inflammation
Role of inflammation - Deliver phagocytic leukocytes to area - destroy invading pathogens / nectroic cells - can result in destruction of healthy cells - secretion of growth factors for repair 1. Recruitment of leukocytes - extravation (vessel - IF) 2. Migration across endothelial + vessel wall 3. Migration in the tissues toward chemotactic stimulus (chemotaxis)

2002MSC Pathophysiology (8 decks)

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