Pathophysiology Test Questions – Flashcards
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Hyperplasia
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Increase in cell number. Cells retain normal structure.
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Causes of hyperplasia
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- hormone signaling (uterine lining) - increased functional workload (increased blood cells due to high altitude living)
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Hypertrophy
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Increase in cell size. Cells retain normal structure.
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Causes of Hypertrophy
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- hormonal signaling (breast cells for lactation) - increased functional workload (weight training, immune activity in lymph)
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Atrophy
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Decrease in cell size. Cells retain normal structure.
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Causes of cellular Atrophy
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- Decreased functional demand - Decreased Oxygen supply (ischemia) - Chronic nutritional deprivation - Halted hormonal or neurological signals
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Metaplasia
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Change of one cell type to another. ie: simple cuboidal to stratified squamous.. IS reversable.
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Causes of metaplasia
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Adaptation to a chronic stressor (esophageal epithelium in GERD patients)
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Ischemia
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Decreased oxygen supply or perfusion to cells / tissues.
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Dysplasia
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change in cell size, shape, uniformity, arrangement, and structure.
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Cause of Dysplasia
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- Response to chronic and persistent stressor - Mutations in DNA
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Anaplasia
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Loss of cellular differentiation, loss of normal cell function. can occur in degrees: more highly anaplastic (completely undifferentiated ) cells are more highly invasive and aggressive/ malignant.
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Causes of anaplasia
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Mutations in DNA resulting in a cancerous, undifferentiated cell type.
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Apoptosis
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Programmed cell death.
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Necrosis
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Death of cells related to cell injury
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cardiac hypertrophy
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excessive workload and functional demand causes the cells of the heart to enlarge to a point detrimental to the heart's function.
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1st barrier to infection is composed of:
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- physical/ mechanical barriers such as skin & epithelia - Biochemical barriers such as antimicrobial peptides and natural flora
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2nd barrier to infection is composed of:
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- Vascular inflammatory response (vessel dilation to dilute toxins, increased permeability permits WBC to exit vascular system etc.)
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cellular mediators of inflammation
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- granulocytes - platelets - monocytes - lymphocytes
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Chemotactic factors are:
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- released by mast cells at site of inflammation - Neutrophil / eosinophil chemotactic factor recruit respective cells to the inflammation site
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oncotic pressure
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osmotic draw of water into vessels - proteins important in this function.
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il-1
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Il-6
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tnf
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il-10
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suppresses immune system
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hyperthermia
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heat cramps
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loss of sodium
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heat exhaustion
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a kind of shock, low plasma volume due to vasodialation
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heat stroke
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brain goes into disfunction. cerebral edema, necrosis & degeneration of brain tissue
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hypothermia
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body temp below 35°c crystals will precipitate out of blood
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blepharitis
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stye
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infection of the gland on the eyelid
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conjunctivitis
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pink eye: bacterial or viral infection urine therapy allergens silver nitrate vs chlamydia in newborns
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strabismus
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deviation in the fusion mechanism where the eyes fixate together.
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nystagmus
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involuntary uni/bilateral movement of the eye.
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amblyopia
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the brain is not processing the images sent from the eye. Often caused by a lack of correct vision early on.
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scotoma
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dark adaptation of the retina
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glaucoma
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open angle - outflow obstruction of aqueous humor; hereditary angle closure - medical emergency: displacement of iris causing obstruction of humor
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macular degeneration
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cells of macula affected dry: yellow age spots / yellow pigment deposits wet: blood vessels trying to form because of diabetes etc.
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alterations of accomodation
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lens loses flexibility
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myopia
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hyperopia
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astigmatism
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otitis media
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otitis externa
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infection of outer ear: prolonged moisture, ie: swimmers ear
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meniere disease
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excess endolymph disrupts hearing function vertigo, nausea, hearing loss
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nk cells
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nonspecific target, attack cancer and virally infected cells
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rheumatoid arthritis
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autoimmune disease rheumatoid factor is a marker causes synthesis of synovial joint material ab vs joint material or circulating ab get deposited there
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respiratory alkylosis
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hyperventilation - too much acid is being blown off kidney compensates by dumping bicarbonate
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respiratory acidosis
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metabolic acidosis
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too much acid in cell, k is forced to leave. Hypokalemia kidneys dump H+ or retain bicarbonate respiratory rate increase to blow off more CO2
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glutamate
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excitatory neuromodulator
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gaba
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inhibitory neuromodulator
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multiple myeloma
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plasma cells cancer bence jones protein anemia destroys bone marrow because too much ab. "punched out lesions" too much protein damages the kidneys
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lymphocytic leukemia
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wbc cancer acute lymphocytic - kids chronic lymphocytic - kids, elderly
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myelogenous leukemia
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acute myelogenous - chronic myelogenous -
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hodgkins lymphoma
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b cell tissue reed-stenberg cells
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non-hodgkins lymphoma
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B, T, nk cells
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neural tube defects
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spina bifida hole in spinal column to lack of brain tissue folic acid prevents condition
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lateral / medial spinothalamic tract
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neo - cortex paleo - brainstem and autonomic
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aldosterone vs ADH
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increase blood pressure by water retention aldostetone: sodium re-absorption at tubules. Licorice ADH: changes permeability to water, retain water in tubule
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upper motor neuron lesion disease
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cerebral palsy
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chromosome translocation
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loss of heterozygosity
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both alleles are affected
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trigger for autonomic disreflexia
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full bladder, distended bowel
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fibrinous exudate
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white, second exudate layer after serous before purulent
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haemorragic exudate
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ulcerative colitis/ crohns, tb, cancer
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ratio of carbonic acid to CO2
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20: 1
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neutrophil recruitment stage
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primary response cell
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macrophage recruitment stage
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end of acute stage
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fibroblast recruitment stage
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chronic inflammation
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reticular activating system
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for arousal, coordinagtion
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meningitis
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arises from ear or nasal infection symptoms include stiff neck (meninges) viral: bacterial: worse prognosis
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acute phase proteins
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produced in liver
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clotting mechanism
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factor 12 thrombin fibrinogen -> fibrin clot plasminogen to plasmin breaks down clot
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angiogenesis
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new vascular development often in the area of cancer development, also in the process of healing VEGF vascular endogenous growth factor
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secondary brain injury
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excess cytotoxicity edema will cause increased pressure, decreased perfusion will result,
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huntingtons disease
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damage to basal ganglia because of decreased gaba production autosomal dominant fatal
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histamine H1 receptor
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pro-inflammatory receptor found in smooth muscle of bronchi etc. Blocked by antihistamines
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histamine h2 receptor
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anti-inflammatory receptor found on the parietal cells of the stomach mucosa.
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leukotrienes
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lipid product of arachadonic acid that has similar activity to histamine but has a slower and more prolonged response.
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prostaglandins
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long chain fatty acids derived from arachadonic acid which cause vascular dilation, neutrophil recruitment and stimulate nerves to produce pain condensation.
