Patho exam 1 Flashcards
Simple Squamous epithelium
location: lining of ventral cavities, blood vessels, alveoli of lungs
function: reduces friction, controls vessel permeability, secretion
Simple cubodial
location: glands and ducts
functions: secretion, absorption, limited protection
Simple columnar
location: lining of stomach, intestine, esophagus, gallbladder
functions: protection, secretion, and absorption
Transition epithelium
location: urinary bladder, renal pelvis of kidney, ureter
Pseduostratified columnar
location: lining of nasal passage, trachea, bronchi
function: protection and secretion
stratified squamous
location: skin, vagina, rectum, anus, mouth, throat
function: protection
Types of hypoxia
- ischemia
- hypoxemia
- failure of oxidative phosphorylation
Ischeima
- blood vessels and/or pumps do not work
- occlusion / pump failure
Hypoxemia
- blood vessels and pumps work fine, but blood does not carry O2 properly
- failure to perfuse or ventilate lungs, lack of RBC, low O2 in blood stream, inability of hemoglobin to bind/release O2
Failure of oxidative phosphorylation
- cells are not using O2 properly
- cyanide, carbon monoxide
Patters of cell injury
- hypoxia
- poor nutrition
- infections agents
- chemical agents
- physical agents
- immune injury
Sources of intracelluar accumulations
- triglycerides
- glycogen
- pigments
- calcium
Dystrophic calcification
- “wrong place”
- calcium phosphate or calcium hydroxide create crystals which create masses
- Normal: pinal glands, airway cartilages, mitral valve, aortic valve
- abnormal: breast cancers, surgical scars, retained abortions
Metastatic calcifications
- occur in abnormal places
- high levels of calcium and/or phosphate
- sites of pH gradients like small airways
Coagulation necrosis
- usually due to ischemic hypoxia for free radical injury EXCEPT in the brain
- death of groups of cells
- DNA gets destroyed but cell membrane stays intact
- replaced by scar, destroyed, walled off, or healed
- has inflammatory response
Liquefactive necrosis
- usually due to a bacterial infection
- death of groups of cells
- no inflammatory response
- results from hydrolysis via lysosomal or WBC enzymes
- cells disappear or leave gelatinous mass
Casous necrosis
- also called saponification
- usually due to immune injury
- death of groups of cells
- crumbled, gross-pale, cheesy
- nucleus disappears, but the cells are not gone
Apoptosis
- programmed cell death
- single cell death
- triggered by mitochondrial damage (leak caspase) or death receptors
- usually due to immune response
- cell membrane stays intact and remains are phagocytized by marcrophages
- no inflammatory response
Dry gangrene
- caused by coagulation necrosis
- large scale death
- no infection
Wet gangrene
- caused by liquefactive necrosis
- large scale death
- foul smelling
- infected
Gas gangrene
- Clotridal gangrene
- flesh eating
Atrophy
- decrease in cell size not cell number
- causes: loss of motor innervation, decreased blood supply, decreased hormonal stimulation, malnutrition
ex: breast after pregnancy, loss of muscle mass in a cast
Hypertrophy
- increase in cell size not cell number
- causes: increased work load, increased hormonal stimulation, normal stress like HTN
- ex: muscle in weight lifters, heart in obese person, breast during pregnancy
Hyperplaisa
- increase in number of cells not size of cells
- causes: compensatory, hormonal stimulation, genetic mutations
ex. female breast during puberty, lymph nodes close to infection, t-cells during infection, bone marrow after giving blood
Metaplasia
- adaptive substitution of one cell type for another
- ex. pseudostratifed epithelium in airway changing to something more durable due to smoking
Dysplasia
- bad growth
- atypical hyperplasia
- loss of cell uniformity and orientation
- resembles cancer, but is not invasive yet
- results from genetic mutation to create a growth advantage
- anaplasia is when it invades
Roles of cells in inflammatory process
- neutrophils: infections caused by common bacteria
- lymphocytes: viral infections
- plasma cells: spirochete disease (syphilis and lyme disease)
- monocytes/macrophages: in TB and fungal infections
- eosinophils: infections caused by worms
Cardinal signs of acute inflammation
- vasodilation: increased blood flow
- neutorphil infiltration: margination, emigration, chemotaxis
- increased capillary permeability: leakage of fluids and proteins
Prostaglandins
- inflammatory mediators
- decrease vascular tone
- increase pain
Thromboxane A2
- a prostaglandin
- produced by platelets
- vasocontriction and platelet aggregation
Prostacyclin (PGI2)
- a prostaglandin
- produced by endothelial cells
- vasodilation, prevents platelet aggreation
Prostaglandin E2
- a prostaglandin
- vasodilation, potentiates bradykinin, fever
Leukotrines
- inflammatory mediator
- smooth muscle contraction
- neutorphil chemotaxis
Leukotriene C4
- increases capillary permeability
- breaks down to LTD4 and LTE4
- causes smooth muscle contractions
Leukotriene B4
-neutrophil and monocyte chemotaxis
Define systemic inflammation
- SIRS
- systemic inflammatory response syndrome
- large production of inflammatory mediators that results in multisystem organ failure
- criteria (2 or more): temp >38 C or <36 C; HR >90bmp: RR >20/min: WBC >20,000 or <4, 000
Transudate edema
- salt water, little to no protein content leakage
- results from alterations in starling forces and lymphatic failure
- ex. heart failure, cirrhosis, liver failure
- caused by: excess total body water, salt/fluid overloading, excess aldosterone, kidney failure, lymphatic obstructions, many vein issues
Exudate edema
- protein rich salt water
- results from overly leaky capillaries
- loose proteins
- ex. inflammation, sepsis, burns
Mechanisms of shock
- hypovolemic shock
- cardiogenic shock
- distributive shock (warm)
- obstructive shock
Hypovolemic shock
-decrease in blood volume
Cardiogenic shock
-pump failure
Distributive shock
-profound vasodilation, lack of venous return
Obstructive shock
-external compression of heart or its outflow
Hypoxic injury mechanism
- lack of O2 stops oxidative phosphorlylation and electron transport chain (edema is early sign as water rushes into cells)
- anaerobic metabolism leads to lactic acid accumulation and pH drop
- Ca+2 ATPase fails
- Ca+2 entry is key step leading to cell death
Gaucher’s disease
glucocerebroside
Tay-Sachs’
ganglioside
