etiology
cause or reason for phenomena// identification of causal factors that acting together provoke a disease or injury
pathogenesis
development of disease in cells, tissues and organs/ from initial stimulus to clinical manifestations
clinicial manifestations
signs of the disease
iatrogenic
cause a result of unintended or unwanted medical treatment
Clinical manifestations
signs and symptoms of a pathophysiologic process
Treatment Implications
an understanding of etiology, pathogenesis, and clinical consequences of a particular disorder may suggest that certain treatments could be helpful
eBP
What are some factors that affect disease patterns?
age, ethnicity, gender, socioeconomic factors, lifestyle considerations, geographic location
What are the levels of prevention?
Primary, secondary, tertiary
Primary prevention
Improved nutrition, housing sanitation
immunizations
education
safety precautions
Secondary (early detection)
physical examinations
self breast exams
amniocentesis
Tertiary Treatment
once a disease is established, medical and surgical treatment
rehab
Homeostasis
fight or flight response due to stressors
Allostasis- overall process of adaptive change necessary to achieve homeostasis
What is stress
a real or perceived threat to the balance of homeostasis
Nervous system
neuropsychological manifestations
nervous tic
fatigue
loss of motivation
anxietoy
overeeating
depression
insomnia
integumentary system
eczema
psoriasis
neurodermatitis
acne
hair loss
cardiovascular system
disturbances of heart rate and rythym
hypertension
stroke
coronary artery disease
repiratory system
increased respiration
asthma
hay fever
gostrointestinal system
gastritis
irritable bowel syndrom
diarrhea
nausea and vomitting
ulcerative collitis
immune syste
immunodeficiency
immunosuppression
autoimmune disease
endocrine system
hyperglycemia
diabetes mellitus
gentourinary system
diuresis
irritable bladder
sexual dysfunction
menstrual irregularity
musculodkeletal system
tension headache
muscle contraction backache
rheumatoid arthritis
inflammatory diseases of connective tissue
endoplasmic reticulum function
synthesis of proteins and lipids
synthesis of membrane components
synthesis of products to be excreted from cell
lipid metabolism and detoxification
golgi apparatus
sends sugars, proteins and lipids to correct place
ribosomes
synthesis of proteins
mitochondria
synthesize atp
what is the difference between lysosomes and peroxisomes?
lysosomes is hydrolytic breakdown of organic waste
peroxisomes is the oxidative breakdown of organic waste
cellular metabolism
ATP synthesis
2 phases of cellular metabolism
anabolism- energy using, synthesis
catabolism- energy releasing, glycolysis, krebbs cycle
krebs cycle
glycolisis happends in the mitochondria
pyruvate which is end product of glycolosis causes formation of CO2
ATP is produced
hydrogen ions are pumped from mitochindria
What are the three asic types of transport proteins
atp driven pumps, carries, channel proteins
active vs passive transport
passive transport: facilitated diffusion
active transport: protein pumps that move solutes/ ions across the membrane agains electrochemical or concentration gradient
membrane transport: sodium-potassuim ion pump
atp must be present
maintains low sodium, high potassium concentrations in the cell
maintains cells volum
controls the solute concentration in the cell
affects the osmotic forces acros the membrane
reversible cell injury: swelling
mild stress: cell will remain normal
first manifestation of injury: hydropic swelling is due to accumulation of water
this results from failure or NA/ K pump- results in too much sodium in cell, will cause organ to swell and enlarg (megaly)
reversible cell injury: intracellular accumulations
accumulation of normal or abnormal intracellular substances: lipids, fats, carbohyddrates, glycogen, proteins
caused by: excessive amounts of normal substances, falulty syntheses results in excessive storage, lack of enzyme to break down substances
cellular adaptation
still reversible, happens with persistant stress
atrophy
decrease in cell size
hypertrophy
increase in cell size
hyperplasia
increasein cell number
metaplasia
conversion of one cell type to another
dysplasia
disorganized appearance of cells
preneoplastic
may be reversible if treated in time
irreversible cellular injury
injury is too severe or prolonged to allow adaptation or repair and reveresal
necrosis
tissue and cell death
intracellular contents are released into bloodstream
ex: myocardial infarction elevated troponin level, gangrene
apoptosis
cells are regulated by cell birth and death
programmed cell death without necrosis
ex: rbc lifespan
Hypoxia
lack of o2 in tissue (ischemmia)
hypoxemia
lack of o2 in blood
Etiology of cellular injury
ischemia, nutritional (alcoholism, low iron)
infection and immunologic
chemical
physical and mechanical
(extreme temps or radiation)
cellular aging
result of a progressive dcline in proliferative and reparative capacity of cells coupled witth exposure to environmental factors that cause acccumulation of cellular and molecular damage
free radical theoyr
resulf of accumulateed metabolic cell damage overtime which leads to cell death
somatic death
entire organism death
brain death
absence of brain stem reflexes
neoplasia
abnormal new growth
Anaplasia
lack of differentiated features in a cancer cell, more changes, the worse the prognosis
metastasis
movement of cancer cell to distant site. always a sign of malignancy
benign tumor
lipoma and adenoma
adenocarcinoma
malignant tumor, glandular tissue
carcinoma
malignant tumor
epithelial tissue, 90% of cancers
sarcoma
malignant tumor mesenchymal tissue
(nerve, bone, muscle)
proto- oncogenes
geneticc makeup of ca,
mutant, overactive gene
tumor supressor genes
normally inhibit cell proliferation
screening guidelines for breast
women 20+ sbe education
20-30 CBE every 3 years
40-50 begin annual mammography
colorectal
women and men 50+ colonoscopy every 10 years
FOBT yearly
prostate
men 50+ PSA and/or DRE
cervix
women 21+ pap test every 1-2 years
cancer-related check
men and women 20+ yearly physical
metastasis spread
fewer than 1 in 10,000 cancer cells that enter circulation wiill survive to metastasize
tumor cells appear to "home" to specific targets
spread through bloodstream or lymphatics
effects of cancer on the body
asymptomatic
pain
cachexia
immune suppression
infection
bone marrow suppression
opportunistic infections
hair loss
sloughing mucosal membrane
WBC lifespans
4-10 hrs in tissues, 6 hrs in blood once released from marrow
rbc
80-120 days once released from the bone marrow
platelet
4-5 days omce released from the bone marrow
normal bone repair
1. removal of damaged base
2. dna polymerase inserts new base using good strand as a template
3. dna ligase repairs nick
myloid
originate from myeloid stem cells
neutrophils, monocytes, rbcs megakaryocytes, platelets
lymphoid
originate from lymphoid stem ceells
t cells, b calls, natural killers
myloid neoplasm
originate in bone marrow stem cells and are released into the blood stream
stimulate the overproduction of one or more cell types
produced cells may be normal or abnormal in appearance or function
chronic myeloid leukemia CML
oveerproduction of granulocytes carrying PHILADELPHIA chromosome leading to reduced apoptotic cell death
insidious onset signs and symptoms
inc granulocyte count
fatigue
weight loss
sweats (hypermetabolic)
bleeding
spleenomegaly with abdominal pain
onset
Acute Myeloid Leukemias AML
group of malignancies of varying myeloid stem cells
presentation of affected cells vary in differntiation and maturation with inc blasts
80 % of adult luekemias
onset usually 6th decade of life
LA 40-50% of children and 20-30% of adults
s & s of aml
abrupt onset
bone pain
anemia
thrombocytopenia
frequent infections esp skin, gi, gu, and respiratory tract
Rx for aml
chemotherapy and new monoclonal antibiotics modalities
lymphoid neoplasms
malignant transformations of lymphoid stem cells
t cells, b cells, nk
lymph tissue- lymphoma
blood- luekemia
Chronic Lymphoid leukemias
usually due to a malignant b-cell precursor that invade lyphoid tissue and bone marrow-- prolonged apoptosis
CLL s & s
bone marrow- anemia and thrombocytopenia
lymphoid tissue- enlarged painless lymph nodes and/or spleen
annorexia
weight loss
fatigue
frequent infections
CLL
indolent onset in 6th to 7th decade
usually diagnosed by accident on routine lab draws
treated with chemotherapy
survival ranges from 8-25 years- often die with instead of the dz
Acute Lymphoblastic luekemias
majority are malignant transformation of b-cells
present as lymphoblastic leukemia
lymphoblasts crowd the bone marrow and suppress the formation of other blood cells
common in children
LA 85% in kids and 30-50% in adults
rx- chemotherapy, bone marrow tran
s&s of all
abrupt onset
bone pain
bruising
fever
anorexia
fatigue
abdominal pain
activity avoidance
Plasma Cell Myeloma (multiple myeloma)
malignancy of b-cells- inc antibody fragments called BENCE JONES proteins
multiple tumor sights- bone, liver, spleen, kidneys, lymph bodies
s&s of multiple myelonoma
most are associated with deposition of the antibody framents in the bone and kidneys
high calcium in blood or urine
renal failure
honeycomb bone
bone pain
fractures
anemia
bleeding tendencies
frequent infections
onset at 40 yrs
higher incidence in males
r
Hodgkin Diseases
malignancies of lymph nodes that produce REED STERNBERG cells from b-cells in association with EPSTEIN BARR virus
supra-diaphramatic-medistinal, cervical, supraclaviculur, axillary
exist in four forms
predictable metastatic pattern
overproduction of other
s&s of hodgkin diseases
painless lymphadenopathy
night sweats
pruritus
weight loss
anorexia
Non- Hodgkin disease
malignancies arising in lymph nodes that originate in any (b, tcells, nk) lymph tissue and do not have the reed-sternberg cells
spreadd early and in unpredictable paths
thought to be associated with some viruses
Burkitt's lymphoma- epstein barr)
LA 50% at
Non- hodgkins disease s&s
present with advanced dz
lymphadenopathy (painless)
fever
night sweats
weight loss
pruritus
infections
joint effusions
Mononucleosis
Ebstein Barr Virus (EBV_ infection
most individuals have been exposed to EBV and have developed some immunity
Mono s&s
exposure to contact with saliva
4-6 week incubation period
pharyngitis
lyphadenopathy
fever
spleenomegaly
heptamegaly
dormant or latent for life
lasts 1-4 months
neutropenia
low (<500 cells/ microliter) neutrophils
results in increased infections
infections can be life threatening
requires protection of individuals- neutrophenic precautions
polycythemias
excessive rbc, wbc, and platelet production
increased blood viscosity
hypertension
thrombosis
mucosal hemorrhage
Polycythemia vera
malignant
secondary polycythemia
chronic hypoxemia
relative polycythemia
dehydration
polycythemia s&s
HA
back pain
weakness
fatigue on exertion
pruritus
dizziness
sweating
visual disturbances
weight loss
parethesias
dyspnea
joint discomforts
epigastric pain
polycythemia rx
contingent on cause
remove the cause
phlebotomy
chemo
myelosuppressive therapy
Three bleeding disorderes
Thrombocytopenia
ITP- ideopathic
TTP- thrombo
Thrombocytopenia
deficient platelets due to:
decreased production
decreased survival time
spleenic sequestration
platelet dilution
thrombocytopenia
folate/ B12 decreases
radiation, chemo, drugs, bone cancer, artificial heart valves
spleenomegaly
hypothermia
massive blood transfusions
infections
DIC
thrombocytopenia s&s
life span is 10 days for normal platelets
petechia
purpura
intracrainal hemorrhage
prolonged bleeding time
rx- remove the cause and transfuse
TTP
thrombosis in small veins lead to deficient platelets
thrombocytosis
excess release of preformed platelets (transient)
paradoxical hemorrhage
peripheral ischemia
polmonary emboli
*too many platelets/ run out of platelets to break down
coagulation disorders
result from:
innappropriate activation of the clotting cascade
inappropriate formation or stabilization of the fibrin clot
Hemophilia A&B
inherited X-linked recessive bleeding
due to factor 8 deficiency (A)
due to factor 9 deficiency (B)
inability to form a fibrin clot
hemophilia A is most common
s&s of hemophilia
prolonged bleeding from trauma
spontaneous bleeding
bruising
hematomas
hemarthrosis
hematuria
GI bleeding
intracrial bleeding
dx- based on history, bleeding times, and factor assay
rx- lifestyle changes, replacement therapy
factor replacement
Von Willebrand Disease
autosomal dominant lack of a carrier protein for factor 8
s&s: epitaxis
rarely hemarthrosis
menorrhagia
gi bleeding
dx- bleeding times and factor assay
rx- desmopressin, hormonal supression, replacement therapy
Vitamin K deficiancy
vitamin k is necessary for several clotting factors
infants are deficient due to a sterile gut
(bacteria produce vitamin K), liver immaturity (process vitamin K) and low dietary intake of vitamin k
s&s of Vitamin K deficiency
melena
hematuria
intracranial hemorrhage
GI Bleeding
Menorrhagia
rx- vitamin k replacement
Disseminated Intravascular Coagulation (DIC)
widespread intravascular thrombosis- widespread hemorrhage to do consumption of coagulation factors
occurs secondary to big stressors
bleeding out of organs
DIC s&s
petechia
ecchymoses
orifice bleeding
needle stick site bleeding
dyspnea
hemoptysis
renal
DIC dx and rx
dx- clinical presentation and a series of coagulation studies
rx- remore/ correct cause
replacement of clotting factors
drug therapies
anemia
disease indicator
low hemoglobin
low rbc- diminshed o2 carrying capacity- tissue hypoxia thus fatigue, weakness, angina, pallor, hypotension, lightheadedness, tinnitus
compensatory mechanisms- inc hr inc rr (lack of oxygen), ventricular hypertrophy
bone p
types of anemias
hemolytic, blood loss, hemoglobinopathies
Blood loss anemias
acute:
normocytic
normochromic
dilutional
Chronic:
Iron-deficiency from depletion of iron
microcytic
hypochromic
Hemolytic anemias
premature destruction of RBC
primarily in the spleen, also in the vascular space
retention of the by products of rbc lysis
increase erythropoieses
inherited or acquired
results in spleenomegaly, jaundice, and bilirubin gallstones
inherited hemolytic anemia
sickle cell anemia and thalessemia
Sickle Cell Anemia
autosomal recessive disorder
abnormal hg- hgs
rbcs sickle under stress/ triggers:
low oxygen, low vascular volume
cold stress
infections
acidosis
extreme physical exertion
vaso-occlusion from cells that clump- severe pain
organ dysfunction
extremeties: necrosis
joints: infarcts
lungs: acute chest syndrome
spleen- inc infections
s&s of sickle cell
homlysis of sickled cells
spleenomegaly
asplenia
hyperbillirinemia
sludging of rbcs
necrosis
infections from necrosis
infection leading cause of morbidity and mortality especiallly before three years of age
rx- avoid triggers
hydroxyurea- stimulate hgf pr
Thalassemia
individuals of mediterranean, asian, or african american descent
deficient hg production and hypochromic microcytic anemia
heinz bodies in the bone marrow impair rbc production
accompanying hypercoaguability leads to strokes and pulmonary emboli
growth re
acquired hemolytic anemia
lysis of rbcs due to exogenous factors
blood transfusions
drugs
chemicals
venoms
certain infections
prothetic heart valvees
burn injuries
vaculitis
anemias of deficient rbc production
result from decreased rbc production
lacking adequate nutrients
failed bone marrow
iron deficient anemia
megaloblastic anemia
vitamin b12 deficiency
folic acid deficiency
aplastic anemia
chronic disease anemias
iron deficiency anemia
iron is recycled when rbcs are broken down
chronic blood loss most common cause
occurs also during growth spurts and pregnancy
s&s:
low H & H (Hg and hemaocrit)
low iron stores
low rbc count
microcytic hypochromic rbcs
Iron Deficiency s&s
fatigue
weakness
palpitations
dyspnea
angina
brittle hair andd nails
increased hr
waxy pallor
megaloblastic anemias
alcoholics
pregnant women
anorexic
megaloblastic anemia
large rbcs owing to folic acid deficiency or vitamin b12 are necessary for dna synthesis
results in weak rbcs
vitamin b12 deficiency anemia is accompanied by neuronal changes that lead to dementia and other neurologic impairment
anaplastic anemia
bone marrow depression leads to low rbc, wbcs and platelets
causes:
radiation
drugs
chemicals
toxins
infection
autoimmune reactions
aplastic anemia s&s
sudden or insidious onset
weakness
fatigue
pallor
petechia
eccochymoses
bleeding
frequent infections
aplastic anemia rx
bone marrow transplant
graft vs host reactions
rbc transfusions
antibiotics
immunosuppresion
chronic disease anemia
renal failure
cancer
chronic infection
aids
rheumatoid arthritis
systemic lupus erythematosus
hodgkins dz