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
ulcerative colitis
autoimmune disease of chronic inflammation of the mucosa in the rectum and proximal colon
-ulceration, obstruction, GI bleeding
ulcerative colitis manifestations
bloody diarrhea, rectal bleeding, abdominal pain, fever, fatigue/weakness, anemia
ulcerative colitis diagnosis/treatment
H&P, endoscopy, radiographs, blood count for anemia
-treatment: drugs, surgery
crohns disease
autoimmune disease throughout the GI tract that causes ulcerations, fibrosis, impaired absorption and obstructions and breakdown of all mucosal layers
crohns disease manifestations/treatment
abdominal pain, diarrhea, malnutrition, random bloody stool, fever, anorexia, malabsorption
-treatment: drugs, surgery
5 types of antibodies
GAMED
IgG-GONE-previously affected
IgA-first line of defense-attacks mucosa
IgM-miserable-active infection
IgE-emergency-allergic reaction
IgD-help B cells
innate immunity
non-specific, no antibodies involved, inflammatory process
adaptive immunity
targeted attack from antibody to antigen, T and B lymphocyte activation
innate immunity cells
neutrophils (phagocytosis), NK cells, marophages
adaptive immunity cells
B cells (memory cells, IgG antibodies) and T cells (CD4 antigen specific cells direct the immune response)
type 1 hypersensitivity reaction
immediate, allergic reactions
type 2 hypersensitivity reaction
antibody-mediated reaction
type 3 hypersensitivity reaction
autoimmune complex reaction
type 4 hypersensitivity reaction
t cell mediated reaction (blood transfusion, transplants)
autoimmunity
failure to distinguish cells that are self vs non-self
-damages organs or entire systems
anaphylactic (allergic) reaction
exaggerated immune response from a type 1 hypersensitivity
-IgE response from previous sensitivity
anaphylactic reaction process
type 1 hypersensitivity/IgE response>mast cell activation>smooth muscle dilation>bronchoconstriction>increased vascular permeability
anaphylactic reaction phases
phase 1: difficulty breathing, skin flushing, itching
phase 2: hypotension, edema, shock, difficulty swallowing
anaphylactic reaction treatment
desensitization (allergy shots), bronchodilators, vasoconstrictors
HIV/AIDS
immunodeficiency from CD4 T-cell infection with HIV (CD4<200)
AIDS process
lost active immune response from CD4s-no direction of immune response, B cells don’t make antibodies
AIDS manifestations
opportunistic infections, immunocompromisation
AIDS diagnosis
CD4 count<200, recurrent infections, HIV antibodies, HIV viral load
HIV treatment
ART-suppresses viral load, preserves immune function, reduces mortality rate
hepatitis
acute/chronic inflammation of the liver from infection
hepatitis types
A, E: bowel: from contact with feces/oral contact
C: circulatory: from contact with blood
B: body fluids: contact with body fluids
D: from infection with B
hepatitis manifestations
hepatocyte death
initially: fatigue, anorexia, fever, RUQ pain, generalized symptoms
developing: jaundice, hepatomegaly (enlarged liver), dark urine/stool
hepatitis diagnosis
blood viral antibody detection, bilirubin in urine, serum bilirubin, blood clotting time
hepatitis treatment
fluids, antivirals, analgesics
UTIs
ascending infections of the urinary tract that causes cell death in the epithelium
-usually from E. coli
cystitis
bladder inflammation
UTI manifestations
dysuria, frequency, hematuria, cloudy urine
-usually localized
UTI diagnosis
H&P, urinalysis, urine culture
UTI treatment
antibiotics, increased fluid intake
pyelonephritis
bacterial infection of the kidneys
-usually an ascended UTI or from E. coli
pyelonephritis risk factors
obstructions (kidney stones), incompetent voiding, frequent intercourse, STIs
pyelonephritis manifestations
flank pain, fever, nausea/vomiting, dysuria, frequent urination, lower abdominal pain, bloody urine
-more systemic manifestations
pyelonephritis diagnosis/treatment
H&P, urinalysis, urine culture
-treatment: antibiotics, surgery, IVs
dehydration&fluid/electrolyte balance
sodium imbalance-hypernatremia or hyponatremia, hypovolemia
dehydration causes
decreased intake, increased output (ex: diarrhea, emesis), fluid shifts (ex: ascites)
dehydration manifestations
decreased LOC, longer capillary refill, changed vital signs, decreased urine output
cirrhosis
liver disease (inflammation/damage) from interfered blood flow and hepatocyte damage
cirrhosis causes
hepatitis or chronic alcohol use
cirrhosis manifestations
altered fluid balance, portal hypertension, ascites, increased girth, increased weight, Na+ retention/hyponatremia, renal failure, jaundice
cirrhosis diagnosis
examination/measurements, ascitic fluid analysis, liver/renal function tests, cardiac function tests
cirrhosis treatment
paracentesis (fluid drainage), diuresis
acid-base balance: plasma, renal, respiratory
plasma: reacts in seconds to H+ levels (acid) with bicarb (base) and K+
respiratory: reacts in minutes to get rid of CO2
renal: reacts in hours/days to make more bicarb (base) and ions
impaired ventilation
blocked airflow in and out of the lungs
causes of impaired ventilation
compression/narrowed airways, disrupted neurotransmission
impaired diffusion causes:
hypoxemia (low blood O2), hypoxia, hypercapnia
pneumonia
inflamed lungs, obstructed bronchioles, and alveoli from fluid accumulation
pneumonia manifestations
productive cough, fever, dyspnea, tachycardia, tachypnea, crackles
emphysema
destroyed alveolar walls from A1 deficiency that obstructs airflow
-air trapping
