EMS lectures 2,3,4, Flashcards

1
Q
What do the following Prefix Mean
Ana-
Dys-
Hyper-
Hypo-
Meta-
A
Without
Disordered
excess
deficiency
change of state
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2
Q

what do the following suffix mean

  • itis
  • oma
  • osis
  • oid
  • penia
  • cytosis
  • ectasis
  • plasia
  • opathy
A

1) Inflammatory Process
2) tumour
3) state
4) resemble
5) reduction
6) increase
7) dilation
8) disorder of growth
9) abnormal appearance, lacking in characteristic

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3
Q

Define cell injury

A

Biochemical and or morphological changes that occur when the steady state of a cell is perturbed by adverse influences

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4
Q

what occurs when cells are put under stress

A

cellular adaption

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5
Q

what types of cellular adaption occurs with increased cellular activity

A

hyperplasia

hypertrophy

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6
Q

what cellular adaption occurs with decreased cellular activity

A

atrophy

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7
Q

what can cause cell injurty

A
O2 availability
trauma
chemical agents
infectious organisms
irradiation
immunological
lack of vitamins/nutrients
genetic disorders
aging
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8
Q

What does hypoxia cause and what is it?

A

reduction or loss of o2 delivery to cells leads to ischaemia

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9
Q

what is Reoxygenation, and what is a risk of it?

A

reperfusion of the ischaemic tissues, can generate free radicals that cause pain

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10
Q

How can physical trauma damage cells

A

disruption of cell structure

thrombosis leads to ischaemia

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11
Q

what are the targets of cell injury

A

mitochondrial function
membrane integrity and function
cytoskeleton
genetic apparatus

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12
Q

what is the result of a sublethal cell injury

A

cell swelling

fatty change - accumulation steatosis

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13
Q

Free Radical toxicity - how it works

A

free radical created in highly reactive ions
stimulates cell injury pathway
chain reaction causes more free radicals
apoptosis of damaged proteins

Detoxification - Vit A,C,E and antioxidants = treatment

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14
Q

what can cause membrane defects?

What does Ca2+ influx cause?

A

bacterial toxins, viral proteins, complement, cytolytic lymphocytes, chemical and physical agents

activated enzymes with deleterious cellular effects

  • APTases - inc ATP depletion
  • phospholipase - membrane damage
  • protease - breakdown membrane and cytoskeleton
  • endonuclease - DNA fragmentation
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15
Q

when does cell death occur

A

when irreversible damage has been done to the interaction between DNA, membrane and enzymes

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16
Q

what is necrosis ?

Types of necrosis - morphological categories

A
cell death as result of lethal cell injury
- passive process
- causes inflammatory reaction 
types 
- coagulative
- caseous - TB 
- colliquative - occurs in brain 
- gangrene 
- fat/fibrinoid
17
Q

Explain Coagulative Necrosis

A

Denaturation of cytoplasmic protein

necrotic tissue swollen and firm
shows evidence of retention in microscopic architecture

Typical ischaemic injury

18
Q

Caseous Necrosis - explain

A

cellular detail is destroyed and area is surrounded by granulomatous inflammation

typical in TB

19
Q

Colliquative necrosis - explain

A

necrotic brain tissue totally liquifies and site is marked by a cyst

20
Q

Gangrenous necrosis - types

A

wet - common in bowel

Dry - common in diabetes

21
Q

What is apoptosis

A

programmes cell death
active and requires damage

can be both physiological AND pathological

22
Q

what is acute inflammation

A

non specific initial reaction to cell damage

23
Q

causes of acute inflammation

A

1) tissue death - (ischaemic, trauma, toxins, chemical insult, thermal injury, radiation)
2) Infection - bacterial especially

24
Q

what are the function of acute inflammation

A

clear away dead tissue
locally protect from infection
allow access of immune system components

25
Q

what are the 4 cardinal signs of inflammation

A

calor, rubor, dolor, tumor

Heat, redness, pain, swelling

26
Q

what is the meaning of the following types of inflammation

  • serous
  • fibrinous
  • purulent
A
  • outpouring of serous fluid
  • fibrin
  • pus
27
Q

what are the components of a inflammatory response (3)

A

vascular reaction - dilation
exudative reaction - formation of inflammatory exudate
cellular reaction - migration of inflammatory cells out of vessels

28
Q

what occurs in the vascular reaction

A

microvascular dilatation
flow inc then decreases
increased permeability of vessels

mediated inc perm
- histamine, bradykinin, NO, leukotriene B4, complement component pass through

Non-mediated in perm
- damage to endothelium
toxins and physical agents pass though

29
Q

What occurs in the cellular reaction

A

accumulation of neutrophils in the extracellular space

severe cases neutrophils and cell debris = pus

30
Q

what is the exudate formed

A

protein rich - filled with immunoglobulins and fibrinogen

constantly turning over
- dilutes noxious agents, supplies nutrients, spreads inflammatory mediators antibiotics and drugs

31
Q

What are neutrophils

Where are they produced

A
  • commonest white cell in blood
  • responsible for directional chemotaxis
  • can move into tissue
  • short life span

produced in bone marrow
PHAGOCYTOTIC

32
Q

cell derived mediators of acute inflammation

A

histamine - stored

synthesised
prostaglandins
leukotrienes
PAD
cytokines
NO
chemokines
33
Q

plasma derived mediators of acute inflammation

A

kinin system
clotting pathway
thrombolytic pathway
complement pathway