Patho- inflammation - acid base imbalance Flashcards
what are the steps of acute inflammation?
Vascular response
cellular response
What is vascular response?
stat brief vasoconstriction
leukocytes, mast cells, and platelets release mediators histamine and prostaglandin
histamine and prostaglandin brings capillary dilation, increase cap permeability,dilates blood vessels and mediates pain
vasodilation increase blood flow to area which causes hyperaemia
increased cap permeability allows exudate to form
fluid and protein shift causing swelling and pain
pain causes immobilization
Vasoconstriction- vs- Vasodilation
Vasoconstriction- clotting occurs during
Vasodilation- brings resources to site
What is hyperaemia?
redness, flushed warm skin
caused by vasodilation
what is a histamine?
a protein that is released by leukocytes, mast cells, and platelets which causes capillary dilation –> chemical response takes longer than euro response
increase cap permeability
dilates blood vessels
what is prostaglandin?
prostaglandin is considered a local hormone
(acts on point of release, does different things at different sites)
brings cap dilation. dilates blood vessels and mediates plain
Why do you need increased cap permeability?
allows exudate to form
what is exudate?
proteins, cells and plasma
what does the fluid and protein shift cause?
swelling and pain
signs of inflammation
redness, warmth, swelling, pain
what do leukocytes, mast cells and platelets release?
mediators- histamine, and prostaglandin
What is the cellular response?
Chemotaxis of neutrophils and other WBC to site
margination on endothelium assisted by adhesion molecules (integrins and selections)
Diapedesis/ emigration into tissue spaces
phagocytosis of cell debris and foreign particles
what is chemotaxis?
movement of an organism in response to a chemical stimulus
what is margination?
process in which free-flowing leukocytes exit the central blood stream, and initiate leukocyte and endothelial cell interactions by close mechanical contact.
what are adhesion molecules
selectin and integrins
Selectins
type of adhesion molecule
integrins
type of adhesion molecule
what is diapedesis ?
is the movement of leukocytes out of the circulatory system, towards the site of tissue damage or infection
what is emigration
same as diapedesis
what are PCAM
platelet cell adhesion molecules
types of exudate?
serous purulent/ suppurative hemorrhagic fibrinous membranous
what is serous exudate ?
watery, decreased proteins of cells
mild, acute inflammation
what is purulent/ suppurative exudate?
pus, WBC, necrotic debris
cloudy, foul odour
severe, acute inflammation
what is hemorrhagic exudate?
RBCs
severe injury
what is fibrinous exudate?
increased number of fibrinogen
forms sticky mesh
what is membranous exudate?
developing mucus membrane
necrotic cells in fibropurulent exudate
systemic manifestations of inflammation ?
malaise, fatigue, headache
fever
what does fever do ?
enhances phagocytosis and triggers immune response
inhibits reproduction and growth of pathogens
why is fever considered good?
enhances phagocytosis and triggers immune response, inhibits reproduction and growth of pathogens
what is the pathogenesis of fever?
Exogenous pyrogens–> endogenous pyrogens–> PGE 2—> hypothalamic receptor–> adj temp to set point via CAMP
what does the hypothalamic receptor do?
adjusts temperature set point via CAMP
What is CRP
C- Reactive protein
Hepatic protein
What does CRP do?
Produced in response to inflammation;
acts as a serum marker, role in defence via complement, non specific marker
has increased levels in atherosclerosis
what are some treatments of inflammation ?
Cold, Elevation, pressure, heat, NSAIDS, steroidal anti inflam drugs
What does cold do to inflm ?
decreases swelling–> increases vasoconstriction, less volume of blood–> decreased pressure –> decreased volume of exudate–> decreased swelling
What does elevation and pressure do to inflam?
decreased blood flow, decreases exudate, decreases swelling
what does heat do to inflam ?
stimulates phagocytosis
what do NSAIDS do to inflam?
decrease prostaglandin synthesis–> decrease in pain
What do steroidal anti- inflame drugs do to inflam?
decrease permeability
decrease WBC and mast cells at site
decrease prostaglandin and histamine release
what are the three types of abnormal immune response?
autoimmunity
hypersensitivity
immunodeficiency
what is immunodeficiency ?
partial or complete loss of immune response
increases risk of disease
what are the types of immunodeficiency ?
primary and secondary immunodeficiency
what is primary immunodeficiency ?
immunodeficiency that is genetic or congenital
what is secondary immunodeficiency ?
acquired or post natal immunodeficiency
is genetic primary or secondary?
primary
types of secondary immunodeficiency
T- cell disorders B- cell disorders T&B- cell disorders Complement disorders phagocytosis disorders
what type of infection could cause secondary immunodeficiency ?
AIDS
causes of secondary immunodeficiency ?
Cancer treatments
infection (aids)
immunosuppressive drugs
What are T cell disorders?
Impaired T cell function
What are B cell disorders?
impaired Antibody production
What are T&B cells disorders
impaired immune function
what are complement disorders?
problems with complement
What are disorders of phagocytosis?
problems with macrophage, and t cells
What are the treatments for immunodeficiency ?
replacement therapy (gamma globulins) marrow/ thymus transplant
What is hypersensitivity?
immune response that is exaggerated or inappropriate
Inflm and tissue damage occurs
what are the types of hypersensitivity?
Type 1- IG E mediated or ALLERGY
Type 2- Cytotoxic Hypersensitivity or tissue specific Hypersensitivity
Type 3- Immune complex Hypersensitivity
Type 4- T-cell mediated Hypersensitivity or delayed Hypersensitivity
What is type 1 or IG E mediated (allergy) hypersensitivity
due to Allergens (drugs, food)
Rapid response
Sensitization of Mast cells;
1st exposure to allergen–> TH2–> B cell stimulation —> IG E forms and attaches to mast cells–> mast cells sensitized
Re- exposure;
Allergen binds to IG E on mast cell —> Mediators are released—> Inflm occurs—> target area becomes red, swollen, and pruritic
examples of IGE mediated hypersensitivity?
allergy, asthma, anaphylaxis
what is the most common type or hypersensitivity?
Allergy or IGE mediated
What is type 2 IGM or IGG mediated hypersensitivity?
Antibodies mis target surface antigens on cells
Antibodies + antigens—> antigen bearing cell destroyed by complement, phagocytosis, and inflam
What is an example of IGM OR IGG mediated hypersensitivity ?
incompatible blood transfusion
What is shock?
actue hypoperfusion due to cardiovascular failure—> tissue hypoxia
What happens during anaphylactic shock?
type 1 hypersensitivity —> mediator release—> excessive vasodilation and increased cap permeability —> circulatory failure, deem, bronchospasm
What happens during septic shock?
vasodilation causes hypotension causes systemic inflm—> multi organ dysfunction
What are antigens bearing cells destroyed by ?
complement, phagocytosis
What is type 3 Immune complex hypersensitivity ?
antigen and antibody form AGAB immune complex–> which is deposited in tissues
often on endothelium
Inflm and tissue damage follows
examples of type 3 immune complex hypersensitivity?
Glomerulonephritis, rheumatoid arthritis
deposits in smaller joints– causing inflam and damage to joints
What is type 4 T cell Hypersensitivity reaction?
macrophage presents antigen to T cell –> T cell sensitized–> cytotoxic T cell—-> destroy of antigen bearing cell —> inflame damage
What are the types of T cell hypersensitivity reaction?
Direct (stat)
delayed ( days)- d/t production of lymphokines
Examples of T cell hypersensitivity ?
TB test
contact dermatitis
What is autoimmunity?
self antigens are normally tolerated–>
self is considered foreign
antibodies target self antigens
Ab+AG= inflm damage and necrosis
how can self tolerance be lost?
abnormal T cell activity–> no T cell suppression
Molecular mimicry—> similar epitope (mistaken identity)
Exposure of previously masked self antigens (by disease)
SLE–> Lupus
what is neoplasia?
abnormal cell growth and differentiation
what is neoplasm?
tumor–> abnormal mass, irreversible growth
what is a benign tumour?
uncontrolled slow growth
may stop or regress
differentiated cells
non invasive in relation to a malignant tumour
What is a malignant tumour?
disorderly, rapid growth
poorly differentiated cells
invasive and damaging
What is cancer?
at least on malignant tumour d/t mutated genes –> primary cause
what is oncogenes?
general term for any gene that causes cancer
for benign tumours what suffix do you use?
OMA
for malignant tumours how do you name them?
Carcinoma—> if epithelium
Sarcome —-> if mesenchyme ( non epithelial tissue after birth)
prefix “ aden”
from glandulary epithelium
prefix “osteo”
bone
methods of spread of tumours
extension and invasion
seeding in body cavities
metastasis via blood or lymph
What is metastasis ?
spread of cancer cells from primary to secondary site
What is the most common site of metastasis ?
lymphatic tissue
then liver, lungs, bone and brain
explain stage 1 metastasis
invades local tissue, embolism enter blood or lymph vessel
explain stage 2 metastasis
travel via blood or lymph
reach area of resistance (cap bed)
attach to suitable site—> cytokines, growth factors
Explain stage 3 metastasis
angiogenesis & cell growth at second site
what is grading of tumours ?
restrictive to extensive
1-4
what is staging of tumours?
clinical criteria, physical assessment at hospital—> using global TNM system
T 0-4 ?
size of tumour
Tx
can’t assess size of tumour
T is
in situ= is in original position
N 0-3
regional lymph nodes
M 0-1
metastasis
TNMx
can’t be assessed
Treatments of cancer?
Radiation therapy Chemotherapy Surgery immunotherapy hormone therapy combination therapy
explain radiation therapy
Necrosis via: free radical production and disruption of DNA bonds
explain chemotherapy
targets cell division, prevents/ slows growth of cells
explain surgery
excise tumour—> take more than malignant cells
explain immunotherapy
uses cytokines and antibodies that stimulates immune response to destroy cancer cells
explain hormone therapy
used for hormone responsive tumours—> disrupts regulatory function
explain combination therapy
mix of above therapies
problems associated with therapy?
difficult to focus on malignant cells only
damage normal cells as well
incidence of recurrence
what are congenital abnormalities ?
any defects present at birth due too developmental errors during gestation
when are you most vulnerable for congenital abnormalities ?
most vulnerable during organogenesis ( 15- 60 days post conception)
critical period different for each organ
what are teratogens?
environmental or maternal facts causing birth defects
examples of teratogens?
Thalidomide– limb reduction defects- 15 - 20 days post conception
alcohol- Fetal alcohol syndrome
malnutrition, cigarette smoke, infections—> rubella virus–> german measles
what are the types of genetic abnormalities?
monogenic
mitochondrial gene
complex trait
chromosomal
What is monogenic genetic abnormality
single gene defect
What are the types of manginess genetic abnormalities?
1a- autosomal dominant –> 50 percent chance of inheriting
1b. autosomal recessive—> 25 percent affected, 50 percent carrier, 25 percent unaffected
1c. X linked recessive
what chance do you have of inheriting an autosomal dominant genetic abnormality?
5o percent chance
What chance do you have of inheriting an autosomal recessive genetic abnormality?
25 % affected
50 % carrier
25 % unaffected
what are complex trait genetic abnormalities?
polygenic, genes and environment component
what are types of chromosomal genetic abnormalities ?
numerical abnormalities
structural defects
explain numerical abnormalities
extra or missing chromosome ( aneuploidy )
or
extra chromosome in a pair ( monosomy)
—> named by chromosome ( down syndrome, trisomy 21)
explain structural defects of genetic abnormalities
inversion
translocation
deletion
Fluid is…?
water and electrolytes
dehydration ( volume deficit ) is
decrease of interstitial and intravascular fluids
dehydration caused by
inadeq intake of fluids
loss due to 3rd spacing
increase skin, renal or gi loss
edema is
increase in fluid volume from vascular space
edema causes
increase of capillary hydrostatic pressure
decrease in colloid op ( pull pressure)
increase cap permeability
obstructed lymph flow
what is 3rd spacing?
when fluid accumulates in trans cellular space such as body cavities, pleural spaces –> not easily exchangeable
why is acid base unbalance so critical?
because it can denature proteins, and some proteins are enzymes, hemoglobin, antibodies
proteins are dependent on narrow ph ranges
arterial blood gases important because?
alkalosis= increase base acidosis= increase of acid
4 types of acid base imbalances ?
Respiratory acidosis
metabolic acidosis
respiratory alkalosis
metabolic acidosis
what is the carbonic acid- bicarbonate buffer
C02+ H20 H2CO3 H(+) + HCO3-
carbon dioxide + water carbonic acid hydrogen Ion + bicarbonate ion
Respiratory imbalance, what is it?
CO2 elimination problems
impaired ventilation–> increase of carbon dioxide pressure—> decrease in ph ( resp acidosis)
excess elimination of carbon dioxide —> decrease of carbon dioxide pressure—> increase in ph ( resp alkalosis )
Metabolic imbalance, what is it?
increase or decrease in acid or base
increase acid/decrease base= Metb acidosis
increase base/ decrease acid= metb alkalosis
Compensation for acid base imbalances ?
Kidney and lung compensate for each other—> normalizes ph
treatment for acid base imbalances
oral and IV sol to normalize PH
treatment of underlying cause
