Pathophysiology Part 2 Chapter 7, 8,14,16,19, 21,24, 26, 31

Front 1

Prions

Back 1

protein particles that lack any type of genome
slowly progress
noninflammatory
neural degeneration
=ataxia, dementia,death
resistant to proteases

Front 2

viruses

Back 2

smallest intracellular pathogen
no organized cellular structure
have protein coat around nucleic acid of DNA or RNA
unable to replicate outside of living cell

Front 3

bacteria

Back 3

have both DNA and RNA
reproduce asexually
no organelles
single chromosomal

Front 4

fungi - 2 groups?
sample diseases?

Back 4

yeast or moulds
ringworm, athletes foot
jock itch

candida overgrowth

Front 5

parasites

Back 5

unicellular with eukaryotic cell makeup(nucleus & organelles)
Ingest eggs or parasite to transmit
scabies, chiggers, lice, fleas

Front 6

agents of infectious diseases

Back 6

microorganisms that are usually not visible to human eye

Front 7

epidemiology of infectious diseases

Back 7

study of factors, events, circumstances that influence transmission of infectious diseases in human populations

Front 8

what does epidemiology of infectious disease focus on?

Back 8

incidence and prevalence
-# of new cases and #c of active cases

source, portal of entry, site of infection,signs & symptoms

Front 9

portal of entry?

Back 9

penetration
direct contact
ingestion
inhalation

Front 10

symtomology

Back 10

collection of signs and symptoms (presentation of disease)

Front 11

steps of Disease Course:

Back 11

incubation
prodromal
acute stage
convalescents stage
resolution stage

Front 12

Virulence factors:

Back 12

substances or products that the infectious agent create that enhance ability of disease

Front 13

toxins

Back 13

alter or destroy the normal function of the host or host's cells

bacteria has 2 types; exotoxins/endotoxins

Front 14

adhesion factors:
evasive factors:

Back 14

adhesion; site specific or cell specific

evasive; blks/damages hosts immune response system

ie; influenza has spikes that adhere to respiratory tract

Front 15

diagnoses;

Back 15

need evidence, signs, symptoms,
lab work; culture, serology,antigens or metabolites made by pathogen

Front 16

serology

Back 16

study of serum

Front 17

treatment

Back 17

aimed to eliminate the infectious organism, promote recovery

ways; antimicrobial, immunotherapy, surgical interventions

Front 18

3 types of abnormal immune responses

Back 18

1-immunodeficiency
2-hypersensitivities
3-autoimmune disease

Front 19

immunodeficiency
2 types; primary/secondary

Back 19

primary: genetic/congenital

secondary: acquired

Front 20

examples of primary;
secondary:

Back 20

primary; thymus deficiency- Tcells don't mature
secondary; viral infection, marrow cancer, chemo drugs

Front 21

types of immune responses

Back 21

1) cell mediated
2) humoral mediated
3)complement disorders
4)disorders of phagocytosis

Front 22

What cells type mediate immune response?

Back 22

Lymphocytes; t cells & b cells

Front 23

what are treatments for immune disorders?

Back 23

replacement therapy, for issues producing antibodies
(gamma globulins)
transplants, for problems making marrow or thymus

Front 24

Hypersensitivities

Back 24

overexagerated or inappropriate immune response
causes inflammation and tissue damage

Front 25

what are 4 types of hypersensitivities?

ACID

Back 25

I- Allergy, IgE mediated hypersensitivity
II- Cytotoxic hypersensitivity
III- Immune complex hypersensitivity
1,2,3=antibody mediated

IV- Delayed or cell mediated hypersensitivity (T-cell mediated)

Front 26

samples of type 1 (allergy sensitivity)

Back 26

allergic reactions
anaphalaxis
asthma

Front 27

steps of 1st response to allergen

Back 27

- allergen enters
- stimulates T-helper cells
- helper T-s stimulate product of antibody (IgE)
- antibodies bind to surface of mast cell
- mast cells are sensitized

Front 28

What happens with 2nd exposure to allergen?

Back 28

allergen will bind directly to mast cell
= inflammatory response or death

Front 29

what are the surface receptors on t-helpers and t-cytotoxics?

Back 29

CD4/CD8

Front 30

4 types of shock?

Back 30

cardiogenic
hypovelemic
obstructive
distributive

Front 31

cardiogenic shock

Back 31

cardiac arrest, inadequate flow

Front 32

hypovelemic shock

Back 32

internal bleeding, external blood loss
lower than normal volume

Front 33

obstructive shock

Back 33

pulmonary embolism, physical obstructive of great vessels= NO blood flow

Front 34

Distributive shock

Back 34

form of relative hypovelemia d/t blood vessel dilation
= poor resistance

Front 35

anaphalactic shock

Back 35

due to severe allergic reaction
type 1 hypersensitivity
allergen binds antibody in mast cell
severe vasodilation, edema, acute immune response
bronchospasm
circulatory failure

Front 36

septic shock

Back 36

due to severe infection
vasodilators released
inflammatory mediators released
systemic response/no longer localized
multi-organ dysfunction/incl; hypotension
can quickly cause death

Front 37

describe type 2 hypersensitivity

Back 37

IgM & IgG mediated, cytotoxic
surface receptors on normal body cells
Ab binds Agin normal immune response
causes normal cell destruction/complement is used to destroy cell
plasma proteins trigger phahocytosis

Front 38

describe steps of type 3 hypersensitivity

Back 38

(problem with the breakdown in the immune complex)
-immune complex passes through blood vessel
-attaches to wall
-when defences see, they destroy it, and normal tissue(blood vessel, joint) = tissue destruction
=inflammation, damage, scar tissue forms
-transcapillary exchange cant happen now

Front 39

describe type 4 hypersensitivity

Back 39

NOT dependent on antibody(T-cell reaction)
-ag is presented to Tcell
-Tcell is sensitized
-cytotoxic T cell is formed to destroy antigen
- inflammation
- destruction of all cells w this antigen

Front 40

helper T cells
cytotoxic T cells

Back 40

essential for turning ON antibody production, activates cytotoxic

kill specific target cells, mediate direct lysis, kills all presenting cells (good or bad)

Front 41

2 types of immune response

Back 41

immediate or delayed

Front 42

what needs to happen in delayed immune response?

Back 42

cytokines/lymphokines need to be produced

Front 43

immunologic tolerance

Back 43

able to recognize non-self from self

Front 44

3 mechanisms of auto immune disorders

Back 44

1)molecular mimicry
2)previously masked self antigens
3)abnormal T-cell activity

Front 45

molecular mimocry

Back 45

microbe shares epitope with our body's cell
antibody is unable to tell diff between self / microbe

Front 46

Previously masked sef antigens

Back 46

infections/autoimmune response may release and damage self-antigens/exposing epitomes of Af that has been hidden by immune
continued activation of new lymphocytes that recognize the previously hidden epitopes

Front 47

abnormal T-cell activity (super antigens)

Back 47

triggers such as endotoxins =activation of large # Tcell

supressor cells are not produced therefore T-cells keep producing other components and attack self
=inflammation & necrosis
ie; systemic leupus erethmatosis

Front 48

neoplasia

Back 48

process of altered cell growth & differentiation
• abnormal growth (mass) is formed and called a neoplasm
• tumor (begnin or metastatic)
• irreversible

Front 49

metaplasia

Back 49

one normal cell type is replaced with anther normal cell type

Front 50

dysplasia

Back 50

a normal cell type replaced with abnormal cell type (pre-cancerous change)

Front 51

anaplasia

Back 51

loss of structural differentiation within a cell or group of cells often with increased capacity for multiplication - cancerous

Front 52

malignanat

Back 52

-cell undifferentiated, with anaplasia and atypical struction that does not resemble cells in original tissue
-the more undifferentiated, the more rapid the growth
-grows by invasion, infiltrates surrounding tissue
-can gain access to bvʼs and lymph channels to metastasize

Front 53

benign

Back 53

well-differentiated cells that resemble original tissue

-progressive and slow, may stop growing or regress
-grows by expansion, without invading surrounding tissues. Usually encapsulated
-does not metastasize

Front 54

cancer causing genes

Back 54

oncogenes

Front 55

proto-oncogenes

Back 55

 -stimulate cellular division
 -if mutated, uncontrolled cell division & growth may occur and cells may turn
-cancerous
 -these genes encode for normal cell proteins such as growth factors

Front 56

tumour supressor genes

Back 56

inhibit cell division
if damaged, cell division is uninhibited

Front 57

DNA repair genes

Back 57

 -checks to see if genetic code is correct & corrects it
 -checks proto-oncogenes and tumor suppressor genes
 -mutations in the DNA repair genes often result in cancers cells being produced
 -this is usually the main target in cancer cells, leading to uncontrolled mutations
-because the proto-oncogenes and tumor suppressor genes are directly affected.

Front 58

carcinoma

Back 58

any malignant tumor derived from epithelial tissue; one of the four major
types of cancer

Front 59

sarcoma

Back 59

a usually malignant tumor arising from connective tissue (bone or muscle etc.); one of the four major types of cancer

Front 60

samples of tumours

Back 60

adenoma; benign glandular epithelium
edenocarcinoma; malignant; glandular epithelium
osteoma; benign tumour in bone

Front 61

how often does a tumour double in size?

Back 61

every 100 days

Front 62

methods of metastasis?

Back 62

1invasion(whereitdevelops)andextension(tosurroundingtissue)
2. seedingviabodycavitiesdistancespread
3. (spreadvia)metastasisviabloodorlymph

Front 63

metastisis

Back 63

1 ̊ to 2 ̊ site - spread of cancer cells
! ! most commonly metastasize to lymphatic tissue, then liver, lungs, bones
! ! then brain (largely supplied with bvʼs

Front 64

stage 1 of metastisis

Back 64

-invades
-tumor grows, enters blood or lymph
-emboli move in vessel
-emboli, chunks of cell break off & grow on nearby tissues(these ones don't really survive)
-one emboli enter the capillary bed and grow, but usually killed

Front 65

stage 2 of metastasis

Back 65

distribution via blood or lymph

terminate travel and grow in area of resistance such as capillary bed or lymph
node

Front 66

stage 3 of mestastasis

Back 66

-angiogenesis: Possesses ability to form new blood vessels to bring nutrients to the secondary tumor

-established and thriving at 2 ̊ site

Front 67

pathogenesis of metastisis

Back 67

1. Primary tumor
2. Metastatic subclone
3. Intravasation occurs (entersbloodvessel)
4. Interactswithlymphocytes
5. Tumorembolusformsandiscoatedwithplatelets
6.Extravasation occurs (tumor exits vessel to settle elsewhere)
7. Angiogensis occurs (tumor generates blood supply)

Front 68

cancer staging - 3 guiding characteristics
TNM

Back 68

1) Tumor – T: refers to the size and physical extent of the tumor
2) Node – N: refers to number of lymph nodes that have been invaded by the tumor
3) Metastasis – M: refers to the presence or abscence of metastases of the tumor cells

Front 69

tumour grading (TNM scale)
# refers to how many lymph nodes infected but extent of involvement

Back 69

when biopsy, graded on histology
I-IV

Front 70

TNMx

Back 70

is tumour but cant be assessed

Front 71

treatment

Back 71

radiation; necrosis via free radicals
chemotherapy; cell division/ inhibits replication
surgery; remove tumour/debulk and use chemo drugs after (combo-therapy)
immunotherepy; vaccination, exposed to potent antigen (ie tb vaccine)
hormone therapy
combination therapy

Front 72

what are w major problems with the therapy

Back 72

resumption of growth ; tumor regrows after 5 years
normal cells targeted- rapid proliferating cells, skin, GI tract etc are all affected

Front 73

transcapillary exchange

Back 73

the primary function of the cardiovascular system. The exchange occurs between the capillary blood and the interstitial fluid surrounding tissue cells.! !

Front 74

hydrostatic pressure
osmotic pressure

Back 74

hydrostatic; always out at arteriole end of capillary
osmotic; always in at venous end of capillary

both are within capillary and interstitual space

Front 75

venous vs arteriole in hydrostatic pressure

Back 75

Venous - hydrostatic pressure is lower, and therefore fluid moves into the vessel
Arterial – hydrostatic pressure is greater than the pressure within the capillary and fluid ! will move out

Front 76

residual fluid

Back 76

excess fluid in interstitial space and is typically picked up by the lymph ! ! vessels, if not = edema

Front 77

dehydration

Back 77

volume deficit

Front 78

causes of dehydration

Back 78

inadequate intake
increases in GI metabolism
Increase in renal output
Increased diaphoresis – fluid lost through skin
loss to third spacing
-eg; tumour is a space occupying lesion – increases hydrostatic pressure

Front 79

3rd spacing (transcellular spacing)

Back 79

Extracellular fluids are distributed between the interstitial compartment (i.e. tissue) and
intravascular compartment (i.e. plasma) in an approximately 75%-25% ratio.

Front 80

example of 3rd spacing

Back 80

severe burns, pancreatitis ; fluid may lead out

Front 81

edema

Back 81

increase in interstitual fluid volume from vascular space
-can be life threatening (brain and lungs)

Front 82

causes of edema

Back 82

increase capillary hydrostatic pressure > excess ISF
decrease colloid osmotic pressure > less pull into blood
-obstructed lymph flow; will not be able to absorb residual fluid

Front 83

hypokelimia/hyperkelimia

Back 83

hypokalemia; decrease in plasma potassium levals
hyperkalemia; increase in plasma potassium

Front 84

hypercalcemia

Back 84

total plasma calcium concentration,

caused alot by malignancy

Front 85

Ph

Back 85

ratio of the bicarbonate base to the volatile carbonic acid

normal Ph is 7.4

Front 86

define acid and base

Back 86

Acid is a molecule that can release an H+ ion
Base is a molecule that can accept or combine w/H+

Front 87

what is the source of metabolic acids

Back 87

fixed acid; not eliminated by the lungs but buffered by the body proteins or extracellular buffers such as HCO3(carbonic acid) and eliminated by the kidney.

Front 88

3 forms of carbon dioxide transport and their contribution to acid base balance.

Back 88

-plasma- H2CO3 formed from hydration of dissolved C02 that contributes to Ph
bicarbonate-carbon dioxde in excess of that which can be carried in plasma
hemoglobin-

Front 89

respiratory acidosis
metabolic acidosis

Back 89

- decreased resp= increased carbon dioxide = decrease ph

-decreased blood ph, decreased production of hydrogen or the inabilty to form bicarbonate in the kindney which leads acidosis in the blood

Front 90

alakalosis of respiratory

metabolic alkalosis

Back 90

increased plasma pH and PCO2, increased H+ excretion and reabsorption

increased plasma pH and HCO3= decreased ventilation and increased PCo2