MT 1 Flashcards
dystrophic calcification
deposit of calcium in damaged tissue (atherosclerosis)
ie normal calcium levels
metastatic calcification
deposit of calcium in normal tissue
necrosis
localized death of cells, tissues, or organ
- uncontrolled
- cell membraine breaks down and contents are released
coaglative necrosis
morphalogic appearance of boiled meet
-most common, due to inactivity of hydrolytic enzymes
liquefactive necrosis
dissolution of tissue
- soft and filled with fluid
- eg brain infarct
caseous necrosis
cheese like necrotic tissue
- limited liquifaction
- seen in TB
fat necrosis
fat deposits that are calcified by enzymes
-white chalky areas
apoptosis
cells shrink into small components and are absorbed by other clls
no contents are released
no inflammatory reaction
function of inflammation
- contain and isolate injury
- destroy microorganisms/toxins
- prepare tissue for healing and repair
- coordinated by vascularized living tissue (ie does not happen after death)
clinical signs of acute inflammation
- redness
- pain
- edema
- loss of function
- heat
histamine
inc. vessel permiability
- released by mast cells
basophils
mast cells in tissue
bradykinin
increases vessal permeability
causes pain
compliment
plasma proteins that kill bacteria
-activated by classical, alternative, or lectin pathways
arachidonic acid derivatives
- from phospholipids in cell walls
- metaboized to form inflammatory substances
what do NSAIDS block?
AA derivative formation
presence of fluid in tissue
edema
transudate
protein poor fluid containing few cells
exudate
protein rich fluid
different types
serous inflammation
fewer cells, clear exudate
fibrinous inflammation
sticky, exudate rich in fibrin
purulent inflammation
pus
rich in neutraphils (due to bacterial infection)
ulcerative inflammation
loss of epithelial lining
inflammaiton extens to surrounding tissue
pseudomembranous inflammation
ulceration and fibrinopurulent exidate
-forms pseudomembrane over the ulcer
herniation
abscess in brain inc. volume in cranium–>brain moves down into foremen magnum
-medulla is compressed
outcomes of inflammation
- complete resolution
- abscess formation-lined in fibrous capsule
- healing by fibrosis and scar formation-normal tissue replaced
- progression to chronic inflammation
chronic inflammation
exudate rich in mononuclear cells (lymphocytes, plasma cells, macrophages present)
examples of regeneration abilities
epithelial cells-high
liver cells-can divide but slower
neurons-can’t
wound healing by first intention
occurs after surgical incision
- scab formation, nutraphils enter and scavenge debris
- formation of granulation tissue
- resorbtion of granulation tissue and replacement by fibrous scar
wound healing by second intention
- gaping wound not closed surgically
- granulation tissue forms and is replaced w/fibrous tissue
- wound contracts with time
keloid
scar that expands beyond site of wound
teratogen
agent that causes fetal abnormality
developmental malformation
results in abnormal features
- 75% of the time the cause is unknown
- can be genetic
achondroplastic dwarfism mode of inheritance
autosomal dominant
examples of teratogens
x rays alcohol thalidomide isotretinoin infectious things: TORCH toxoplasmosis (parasites), other (bacterias) (STD, unpasturized milk), Rubella, cytomegaalovirus herpes simplex
fetal alcohol syndrome
- intra-uterine growth retardation
- reduced mental processes
- altered physical appearance
monosomy
loss of chromosome
-autosomal monosomies are fatal
-Y is fatal
X is not- turner’s syndrome
trisomy
presence of extra copy of a chromosome
not necessarily fatal
-sex are usually not lethal
downs syndrom
1 in 800 neonates affected
- complete copy in most cases (more severe phenotype)
- translocation sometimes
- usually the mother’s chromosome, risk is inc. with inc. age
- screen older mothers
- significant morbidity and increased mortality
- intestinal atresia, heart defects, etc.
turner’s syndrome
monosomy X
1 in 3000 neonates
abnormal segregation of X or Y during meiosis
-female but infertile
-ovaries present but unable to produce eggs
klinefelter’s syndrome
trisomy X 1 in 700 neonates -abnormal X or Y segregation -male phenotype (XXY) -infertile-atrophic testis
XXX
still compatible with life
-slowed mental processes
q 13 deletion
q means long arm
known to cause retinoplastonas
alleles
genes present on autosomes
- 1 copy form each parent
- one copy of Y genes for males
marfans pattern of inheritence
autosomal dominant
familial hypercholesterolemia pattern of inheritence
autosomal dominant
what is variable penetrance?
variable expressivity?
the percentage of intividuals with a gene that will actually express it
-degree of expression in the individual with the gene
marfan’s syndrome
defect in fibrillin gene -tall, thin, loose joints -cardiovascular abnormalities -occular abnormalities -shortened life expentancy (usually due to rupture of a dissecting aneurysm)
dissection
blood tracking through vessel vall
familial hypercholesterolemia
defect in LDL receptor gene
-insufficient removal
-deposits in tissue as atheroslerosis and xanthomas in skin and soft tissue
worse phenotype if homozygous
-develop ischemic heart disease before age 20
cystic fibrosis mode of inheritence
autosomal recessive
-carrier rate 1 in 25
cystic fibrosis
defect in Cl transport gene -->thick exocrine secretions that obstruct ducts and cause infections meconium ileus (failure to pass meconium) -pseudomonas nifections
lysosomal storage diseases
- group of diseases of defects in different enzymes
- results in accumulation of materials in lysosomes
- eg lipidoses, glycogenoses
tay sachs
autosomal recessive lysosomal storage disease -defective hexosaminidase -brain, eye changes -3-5 yr life expectancy
gaucher disease
lysosomal storage disease
defective glucocerebrosidase
-enlarged spleen, anemia
-normal life expectancy if type 1
phenylketonuria
defective phenylalanine hydroxylase gene
- which converts it to Tyr
- accumulation causes toxic effects on cells during development (not adulthood)
- can minimize effects by following phenylalanine deficient diet
hemophilia
x-linked recessive-only males are effected
defect in coagulation proteins (clotting factors)
-secondary complications are arthritis, joint malformation
-treatment=factor replacement
duchenne and backer’s muscular distrophy
due to defective dystrophin protein
- which is involved in attachment of cytoskeleton, especially muscles
- duchenne more severe, earlier onset of muscle wasting
fragile x syndrome
affects males (but not classical inheritence pattern)
- portion of X chromosome is fragile due to CGG triplet repeats
- these increase with each generation and mental retardation and enlarged testis are eventually expressed
2 examples of multifactorial inheritence disorders
dysraphia
diabetes type 2
5-10% chance of developing disorder b/c of exogenous and endogenous factors contributing to expresion
egs of dysraphias
=neural tube defects anencephaly-abscence of brain spina bifida-defect in vertebral bones (dont fuse properly) meningocele-defect in vertebre/meninges folate decreases risk
chorionic villus sampling
- biopsy of placental villus
- gets fetal cells for analysis
- risky
premature baby
delivered b/f 37 wks
Intrauterine growth restricted baby
is less than 3200g
immature baby
both premature and low weight
causes of prematureity
maternal-smoking, substance abuse, malnutrition
- fetal-genetics
- placental-insufficiency
neonatal respiratory distress sydrome
shortness of breath
-inadequate surfactant leads to atelectasis and hyaline membrane formation
to treat: release surfactant into amniotic fluid before birth and corticosteroids
igA
present in secretions, milk
as dimer
IgE
present in tissue on mast cells
-mediate alergic responses
IgD
on B cells
activation of lymphocyte
IgM
present in blood
first defense against common bacteria
pentamers
neutralize and activate compliment
IgG
present in blood but indicates later response (B cells make IgM first)
acts as opsonin
type II hypersensitivity
exaggerated immune response from deposition of Ab on cells or tissue
-eg myesthenia gravis
hemolytic anemia
type II hypersensitivit
Abs to protein on surface of RBCs
could be b/c of a drug
graves disease
=autoimmune thyroiditis
Ab against TSH receptor
-hyperthyroidism
myasthenia gravis
Ab against acetycholine receptor on mm
-muscle weakness
type III hypersensitivit
exaggerated immune response from creation of Ag-Ab complexes cauing inflammation in various places
-eg lupus, rheumathoid arthritis
one theory of how lupus works
maybe from defective clearance of cells resulting in Abs against cell parts (eg anti-nucleus)
type IV hypersensitivity
excessive, prolonged immune reaction by immune cells-Ag complexes
-supermacrophages
-possible granulomas
eg tuberculosis
allograft
xenograft
donor
different species donor
hyperacute rejection
w/in hours
due to preformed Ab (usually blood type)
acute rejection
w/in days
Ab and cell mediated
chronic rejection
w/in monts to years
ab and cell mediated
vascular obstruction and tissue destruction
neoplasm
mass of abnormal cells growing autonomously
benign neoplasm
generally well differentiated slow growth no invasion -smooth boarder, encapsulated no matestases
premalignant
likely to become malignant but has not invaded basement membrane
benign epithelial neoplasms
adenoma (some are premalignant, but usually not skin ones)
papilloma
malignant epithelial neoplasm
adenocarcinoma
squamous cell carcinoma
transitional cell carcinoma
in situ (neoplasm nomenclature)
means premalignant
needed to distinguish from truly malignant
sarcoma
malignant neoplasm
carcinogens
substances that produce cancer
inherited cancer syndromes
mutant gene that increases risk of cancer developing
-eg defective DNA repair syndromes
example of a benign tumor associated w/increased risk of malignancy
villous adenomas of colon
grade of malignant neoplasm
describes degree of differentiation
high grade don’t look like cells (poorly differentiated)
low grade are well differentiated
stage
amount of malignant neoplasm
- size
- lymph nodes
- distant metastasis
example of fatal benign neoplasm
meningioma
paraneoplastic syndromes
not explained but happens in cancer patients
- hypercalcemia
- cushing’s-prod of ACTH
- inappropriate antidiuretic hormone produced by Tumor (ADH)
pro-carcinogen
must be modified in body to become a carcinogen
UV radiation
damages DNA
-xeroderma pigmentosa=genetic defect in DNA repair enzymes, leads to early skin cancer
ionizing radiation
leukemias inc. in Japan
thyroid cancer in patients who received radiation to neck
oncogenes
mutated genes whose products are associated with formation of neoplasms
- ie control cell growth
- tumor suppressor genes
water distribution in body
2/3 in intracellular fluid compartment
1/3 in extracellular fluid compartment
–3/4 in interstitium, 1/4 in tissue
edema
accumulation of fluid
-exudate if inflammation, transudate if not
hydrostatic pressure
forces water out
oncotic pressure
pushes water in
anasarca
generalized edema
-fluid accumulates in low areas (ankles or ileosecal region if lying down)
hydrocardia
excess fluid in pericardial cavity
hyperemia
inc. in volume of blood in tissue
-active=from exercise or inflammation
passive-from dec. venous pressure that occurs w/impaired outflow of blood
cyanosis
blue lips and skin due to lack of oxygen
purpura
bruise greater than 3mm
patechiae
pinpoint hemmorhages from capillary rupture
hemoptysis
coughing blood
hematemesis
vomitting blood
hematochezia
blood in rectum (bright red)
melena
dark blood in stool
hematuria
blood in urine
manorrhagia
excessive blood loss in menses
massive blood loss
hypovolemia and shock
clot formation predisposing factors
blood not flowing properly
hypercoaguable state
endothelial injury
embolus
any circulating material that may cause a problem
stenosis
narrowing
causes of shock
S-septic from bacteria H-hypovolemic O-obstructive (eg cardiac tampenade) C-cardiogenic-heart not contracting K-anaphalactic shock S-spinal/neurogenic (lack of or improper innervation)
which vessels don’t have media (smooth muscle)
capillaries and lymphatics
which layer is thickened by age in blood vessels?
intima
arteriosclerosis
atherosclerosis
=intima is scarred (typically by hypertension)
fatty expansion of intima happens
media disease
dissection
raynauds disease-abnormal response to cold and blue cold extremities
vasculitis
which layers does an aneurism effect and what is it?
dilation of vessel wall that predisposes to clot and rupture
effects any or all layers
ischemic heart disease
- reduced coronary circulation (usully from atherosclerosis)
- variable symptoms including: angina, myocardial infarct (death of heart muscle), can become chronic
- arrythmia from ischemia in conduction system
complications of MI
- myocardial rupture-5-7 days after MI, can result in cardiac tampenade
- papillary muscle rupture with mitral regurgitation
- ventricular aneurysm
- arrythmias
- mural thrombus and emboli
congestive heart falure
heart unable to pump enough blood to meet tissue demands
- various causes, including chronic ischemic damage
- shortness of breath, tiredness, etc.
- can’t get blood out to system so accumulates in lungs
- can’t get blood to lungs so it accumulates in veins
dilated cardiomyopathy
dilated chambers
-due to genetics, viral infection, alcohol, late ishemic disease, and chemo
hypertrophic cardiomyopathy
thickened walls-genetic
restrictive cardiomyopathy
reduced ventricular contractility
- idiopathic primary form forms in kids
- aquired forms in adults (eg amyloidosis)
arrythmogenic cardiomyopathy
fibrofatty replacement of myocardium-genetic
septal wall defect
simple defect
tetraology of fallot
cyanotic defect
valvular heart disease
can be stenosis or insufficiency of any valve
-genetics, infection,, autoimmune, etc.
endocarditis
- inflammation of inner heart lining (usually valve)
- sometimes autoimmune or metastises related
- impaired valve function and emboli
myocarditis
inflammation of heart muscle
- including lymphocytic mycarditis, sarcoidosis, eosinophilic myocarditis
- can have long term sequalae of heart failure
- can be caused by viruses, toxins, autoimmunity, medication
pericarditis
inflammation of epicardium and or pericardium
-pericardial effusion and possible tamponade
-can acute-fibrinous
or chronic-fibrous or a mix
-surgery if causing tampenade
cardiac neoplasms
- most commonly metastasis
- typically rapidly fatal
- most common primary cardiac neoplasm is myxoma
anthracosis
accumulation of carbon particles in lungs
-stored as anthracotic pigment
diptheria
bacterial infection in throat that forms membrane
membranes can break off and get inhaled and cause death
parainfluenza virus causes
croup in kids younger that 3
acute epiglottitis
3-7yr old kids
- may cause swelling/closure of airway
- usually self limiting
- immunization
bronchiolitis
kids less than 2 years old
-inflammation due to virus
usually respiratory syncitial virus
difference b/t atypical and typical pneumonia
atypical has nonproductive cough
-infection is in b/t alveoli in interstitial tissue
community aquired vs. hospital aquired causes of pneumonia
community usually gram +
hospital usually gram -
complications of pneumonia
pleuritis
pyothorax-puss in pleural cavity
empeyma-localized areas of pus in pleural cavity
abcess
bronchiectasis-continued inflammation and expansion
chronic lung disease
where does TB initial infection occur?
in the lung, causing Ghon complex to form w/lung lesion and enlarged hilar nodes
common comorbidity of TB
liver disease from antibiotics
egs of obstructive diseases
asthma
COPD
bronchiectasis
cystic fibrosis
extrinsic asthma
intrinsic asthma
attacks precipitated by triggering allergens
attacks precipitated by non-immune mx (eg exercise, stress, temperature)
hypersensitivity pneumonitis
=immune reaction to various organic materials (eg pigeon poo)
-can become chronic and cell-mediated, which leads to destruction and dec. compliance
pneumoconioses
due to inhalation of inorganic dusts (eg sand, coal)
sarcoidosis
multisystemic, unkown etiologies
- non caseating granulomas in various organs
- biopsy to diagnose
- no specific treatment but steroids
aletactasis
expansion of alveoli
adult respiratory distress syndrome
acute respiratory failure that doesn’t respond to oxygen
- ie are still breathing but not oxygenating blood
- injury to lung causes leakage from capillaries
pneumothorex
air into pleural cavity with collapse of lung
pleural effusion
accumulation of fluid in pleural cavity
