Patho exam 1 Flashcards
Hydrostatic pressure
Pressure that drives fluid out of the blood
Osmotic pressure
Pressure that drive fluid back into the vessels
Aldosterone
Released to lower BP
Regulates BP, bv, increase Na absorption
Hyperaldosteronism
Excess aldosterone
Leads to hypernatremia, hypokalemia, hypertension, metabolic acidosis
ADH
Anti-pee hormone
Raises BP and BV
RAAS
Increase BP by activating agiotensin 2 which activates aldosterone
Hyponatremia
Too little Na
Caused by: decreased Na intake, diuretics, vomitting/diarrhea/sweating, too much fluid, CHF or Renail failure
Addison’s
Decreased aldosterone, peeing out all the sodium
SIADH
Increased ADH, retaining too much water
Hypernatremia
Too much Na
Caused by: hypersonic solution, not drinking water, loss of water, diabetes insipidus (excess urination), increased sodium intake
Hyperkalemia
Too much K+
Addisions
renal failure
burns/tissue damage (K leaks into blood)
ACE inhibitors
atrophy
decrease in size of cell
ex: muscular dystrophy
hypertrophy
cardiac muscle that gets bigger and bulkier in disorganized fashion
damages heart
hyperplasia
increase the number of cells
beneficial in mammary glands to prep for breast feeding
metaplasia
cell type changes during times of stress to resist chemical changes
ex: intestinal metaplasia causes cells in upper repiratory tract to change to be able to resist the acidity of stomach acid
dysplasia
disorganized cell growth
cells dont look like each other
not necessarily cancer but can become malignant
ischemia
lack of blood flow
cant deliver glucose throughout the body
cant excrete waste
hypoxia
lack of oxygen
innate immunity
born with
immediate response to harmful agents
nonspecific: macrophages, NK cells, fever, inflammation NOT enought ot contain infection
adaptive immunity
develop over time
LYMPHOCYTES
ID, attack, reinforces, and amplifies immunity
delayed response to specific antigens
T and B cells
T cells (cell mediated)
protect from infections thatve reached inside cell
actually attacks pathogenic cells
CD4 T cells
help macrophages break apart and grab bacteria
help b cells make antibodies (IgG, IgA, IgE)
CD8 T cells
cytotoxic
kills infected cell (can kill cancer cells)
phagocytes clean up afterwards
B cells (humoral)
-provide immunity in fluid by secreting antibodies to circulate throughout the blood
-antibodies that bind to pathogen block infection
-marks the cell so phagocytes know to destroy it
Mast cells
key to inflammatory response: histamine, heparin, serotonin, proteases
effects of histamine
increase capillary permeability
vasodilation
bronchoconstriction
increase nasal mucus secretions
stimulates sensory receptors
5 cardinal signs
heat
redness
swelling
pain
loss of function
anaphylaxis
Type 1 hypersensitivity
EXTREME allergic response
food allergies, antibiotics, latex, insect venom
anaphylaxis symptoms
edema, itchiness
hoarseness, wheezing, flushed airway obstruction
Type 1 hypersensitivity
IgE
immediate reactions
1st exposure= sensitization
subsequent exposure= serious reaction
contraction of bronchi, vasodilation
type 1 hypersensitivity clincal presentation
hives, eczema, allergic rhinitis, asthma, anaphylactic shock
type 1 hypersensitivity treatment
antihistamine
corticosteroids (decrease inflammation)
epinephrine (constricts blood vessels)
type 2 hypersensitivity
IgM and IgG attach to self-reactive cells
occurs when self-reactive cells arent destroyed while maturing (attack healthy cells)
type 2 hypersensitivity: cell lysis
membrane attack complex punches holes into cell allowing fluids to flow in and out
cell bursts and dies
incites inflammatory process and destroys basement membrane
typer 3 hypersensitivity
-mediated by immune complexes
-binding of antigen and antibody forms clumps that don’t get cleared out
-get filtered into the wrong areas
-gets stuck in basement membrane
-Common site: kidney
type 3 hypersensitivity clinical presentation
chills, fever, rash, urticaria, arthritis
ex: post-strep glomerulonephritis
type 4 hypersensitivity
mediated by T cells
delayed response: t cells take time to ramp up
antihistamines don’t help because its mediated by T cells
ex: poison ivy
passive immunity
transferred from another source
ex: mom donates antibodies to babies
active immunity
own immune system responds to something
ex: antibodies develop in response to infection or vaccine
antigen testing
tests for antigen from a pathogen
once infection clears, positive result will disappear
antibody testing
doesn’t indicate infection, indicates exposure (prior illness, vaccine)
maintains positive result even if not sick
PCR tetsing
detects presence of genetic material of pathogen
amplifies RNA/DNA sample
helper T cell deficiency
conduct whole immune response
amplifies phagocytosis and tells T & B cells what to do
deficiency= unable to fight pathogen
susceptible to opportunistic pathogens
HIV transmission
semen, blood, breast milk, contaminated needles, mother to baby
untreated HIV
low CD4
high Viral load
turns into AIDS in 8-10 years
symptomatic HIV
flu like symptoms 1-2 weeks post exposure
Implications of HIV
pregnancy: risk if spreading to child during birth and via breast milk
ART therapy
reduces viral load to undetectable levels
combo of many HIV meds
HIV: Risk of cancer and Opportunisitc infection
suppressed immune system causes increased susceptibility to opportunistic infections
unable to fight cancer
hypokalemia: cause
cushing’s (increase Na+, decreased K)
starvation/vomiting
too much insulin (moves K out)
hypokalemia: symptoms
Lethargic
Low shallow resp
Lethal cardiac rythms
Lots of Urine
Leg cramps
Limp muscles
Low bp/hr
hyperkalemia: symptoms MURDER
muscle weakness
urinary output little/none
resp failure
decreased cardiac contraction
early muscle twitch
rhythm changes (peaked T waves, prolonged PR)
hypocalcemia: cause
decreased PTH (throdiectemy)
decreased intake (lactose intolerance)
decreased vitamin d (helps absorb Ca+)
chronic kidney disease (wastes Ca+)
hypocalcemia: symptoms CRAMPS
convulsions
reflexes hyperactive
arrhythmias (prolonged QT)
muscle spasms
positive signs
sensation of tingling/numbness
hypercalcemia: cause
hyperactive PTH
increased vitamin D
cancer that spread to bone (leaks Ca+ to blood)
lithium (impacts PTH)
hypercalcemia: symptoms WEAK
Weakness of muscle
EKG changes
Absent reflexes/altered mental state/ ab distension
kidney stones
metabolic compensation
release or pick up H
acidosis: too much H+, so release hypervent
alkalosis: too little H+, pick uphypovent
respiratory compensation
increase or decrease resp rate
#1 source of acid in body is CO2
respiratory acidosis
build up of CO2 ( greater than 45)
kidneys compensate by increasing bicarb
respiratory acidosis: cause DEPRESS
drugs/disease of neuromuscular
edema
pneumonia
respiratory center of brain damaged
emboli blocks gas exchange
spasms of bronchial tubes
sac elasticity of aveolar
respiratory alkalosis
no enough CO2 (less than 35)
kidneys compensate by decreasing bicarb
respiratory alkalosis: cause TACHYPNEA
temp increase
aspirin toxicity
controlled mechanical ventilation
hyperventilation
hYsteria
pain/pregnancy (3rd tri)
neurological injuries
embolism and edema
asthma due to hyperventilation
metabolic acidosis
acid build up in body fluids
increased acid production (diabetic keto acidosis)
decreased acid secretion (renal failure)
resp compensates by hyperventilating to expel CO2
metabolic acidosis: ACIDOTIC
Aspirin toxicity
carbs not metabolized- lactic acid
insufficient kidneys
diarrhea
ostomy drainage
fisTuals
carbonic anhydrase inhibitors (diuretic)
metabolic alkalosis
excess loss of acids
resp compensates by hypoventilation to increase CO2
metabolic alkalosis cause ALKALI
aldosterone production excessive
loop diuretics
alkali ingestion
anticoagulant “citrate”- massive blood transfusion
loss of fluids
Increased sodium bicarb admin
characteristics of cancer cells
rapid growth
invasive
not encapsulated
high mitotic index
poorly differentiated
metastasis
Tumor suppressor
behaves as the “breaks”
slows down cell division
repairs DNA mistakes
communicate apoptosis
oncogenes
mutated proto-oncogenes
promote cancer
accelerated cell division
parenoplastic syndrome
rare disorders triggered by abnormal immune system response to cancerous tumors
paraneoplastic examples
Cushings, SIADH, hypercalcemia, hypoglycemia, carcinoid syndrome, polycythemia
angiogenesis
formation of new blood vessels
tumors give off chemical signals to stimulate angiogenesis to feed the tumor
diabetes melitus
cause hyponatremia
glucose pulls all the water into the blood which dilutes the sodium content
diabetes insipidus
excess urination
