Final Exam Flashcards
cellular hypertrophy
cell growth in response to increased demand
cellular atrophy
cell shrinking in response to cell injury
-reversible
cellular hyperplasia
increased cell count in response to increased demand
cellular dysplasia
rapid cell division in no order in response to cell injury/stress
-abnormal
-precursor to cancer
cellular metaplasia
cellular replacement in response to stress/cell injury
-reversible
cell death
necrosis or apoptosis (programmed cell death)
cardiac hypertrophy
increased cardiac size/mass
cardiac hypertrophy reasons
increased LV workload, increased demand, genetics
primary cardiac hypertrophy
inherited, genetic, no EKG changes
secondary cardiac hypertrophy
from an underlying condition that increases LV workload and increased myocardial cell size
cardiac hypertrophy manifestations
obstructed outflow: shortness of breath, chest pain, syncope, impaired function
-asymptomatic usually until cardiac arrest
cardiac hypertrophy diagnostics
genetic testing, hypertension, reduced exercise tolerance, arrhythmias, murmurs
cardiac hypertrophy treatment
surgical, pharmacologic, activity restriction
cervical metaplasia and dysplasia
found in the transformation zone of the cervix-precursor to cervical cancer
-asymptomatic
-pap smear testing, HPV test, biopsy
-usually from HPV, smoking
lines of defense for inflammation
first line: skin, mucous membranes
second line: inflammatory response
third line: immune response
acute inflammation results from
from tissue injury
acute inflammation process
-increases blood flow to injury site
-vasodilators (ex: histamine) and capillary permeability increased
-cell mediators: chemotaxis, adherence, migration, phagocytosis
5 signs of acute inflammation
redness, heat, swelling/edema, pain, decreased function
-systemic manifestations: fever, increased leukocyte/protein count
acute inflammation treatment
reduce blood flow, decrease swelling, stop chemical mediators (ex: anti-histamines), decrease pain
chronic inflammation
inflammation lasting several weeks or longer
-macrophages, lymphocytes involved
-granuloma, scarring formation
-ex: immune disorders, arthritis
acute gastritis causes
irritating substances, poor gastric perfusion
-chronic NSAIDs, aspirin use
-smoking
acute gastritis
acute inflammation of the gastric mucosa
acute gastritis process
gastric epithelium necrosis>acid erodes underlying tissue
acute gastritis manifestations
abdominal pain, indigestion, anorexia, nausea/vomiting, bloody stool, anemia
chronic gastritis
chronic infection/autoimmune disease that leads to chronic inflammation of the gastric mucosa
-usually H. pylori bacteria
chronic gastritis manifestations
mucosa atrophy, impaired gastric acid production, dyspepsia, anorexia, vomiting, anemia
-can be asymptomatic
chronic gastritis diagnosis
endoscopy, biopsy, blood protein test
acute gastritis diagnosis
endoscopy, stool analysis for blood, blood count for anemia
chronic gastritis treatment
PPIs, antibiotics, vitamin B12 supplements
acute gastritis treatment
stop irritating substances, antacids
peptic ulcer disease
area of mucosal inflammation/erosion/breakdown and ulceration
-acute or chronic
-superficial or deep
-usually in duodenum/stomach
-gastric or duodenal
peptic ulcer disease cause
excessive acid secretions, disrupted mucosal barrier, H. pylori infection, smoking, chronic NSAIDs/aspirin use, stress, or alcohol
peptic ulcer disease treatment
PPIs, gastric resection, surgery if severe
peptic ulcer disease manifestations: gastric or duodenal
gastric: anorexia, pain with eating and after meals
duodenal: well nourished, pain on an empty stomach and helped with food