EMS lectures 2,3,4, Flashcards Preview

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Flashcards in EMS lectures 2,3,4, Deck (33):
1

What do the following Prefix Mean
Ana-
Dys-
Hyper-
Hypo-
Meta-

Without
Disordered
excess
deficiency
change of state

2

what do the following suffix mean
-itis
-oma
-osis
-oid
-penia
-cytosis
-ectasis
-plasia
-opathy

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

3

Define cell injury

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

4

what occurs when cells are put under stress

cellular adaption

5

what types of cellular adaption occurs with increased cellular activity

hyperplasia
hypertrophy

6

what cellular adaption occurs with decreased cellular activity

atrophy

7

what can cause cell injurty

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

8

What does hypoxia cause and what is it?

reduction or loss of o2 delivery to cells leads to ischaemia

9

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

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

10

How can physical trauma damage cells

disruption of cell structure
thrombosis leads to ischaemia

11

what are the targets of cell injury

mitochondrial function
membrane integrity and function
cytoskeleton
genetic apparatus

12

what is the result of a sublethal cell injury

cell swelling
fatty change - accumulation steatosis

13

Free Radical toxicity - how it works

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

14

what can cause membrane defects?
What does Ca2+ influx cause?

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

15

when does cell death occur

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

16

what is necrosis ?

Types of necrosis - morphological categories

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

Explain Coagulative Necrosis

Denaturation of cytoplasmic protein

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

Typical ischaemic injury

18

Caseous Necrosis - explain

cellular detail is destroyed and area is surrounded by granulomatous inflammation

typical in TB

19

Colliquative necrosis - explain

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

20

Gangrenous necrosis - types

wet - common in bowel
Dry - common in diabetes

21

What is apoptosis

programmes cell death
active and requires damage

can be both physiological AND pathological

22

what is acute inflammation

non specific initial reaction to cell damage

23

causes of acute inflammation

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

24

what are the function of acute inflammation

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

25

what are the 4 cardinal signs of inflammation

calor, rubor, dolor, tumor

Heat, redness, pain, swelling

26

what is the meaning of the following types of inflammation
- serous
- fibrinous
- purulent

- outpouring of serous fluid
- fibrin
- pus

27

what are the components of a inflammatory response (3)

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

28

what occurs in the vascular reaction

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

What occurs in the cellular reaction

accumulation of neutrophils in the extracellular space

severe cases neutrophils and cell debris = pus

30

what is the exudate formed

protein rich - filled with immunoglobulins and fibrinogen

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

31

What are neutrophils
Where are they produced

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

produced in bone marrow
PHAGOCYTOTIC

32

cell derived mediators of acute inflammation

histamine - stored

synthesised
prostaglandins
leukotrienes
PAD
cytokines
NO
chemokines

33

plasma derived mediators of acute inflammation

kinin system
clotting pathway
thrombolytic pathway
complement pathway