midterm Flashcards
Hydropic
(reversible cell injury)
- accum of water
- *1st manifestation of most forms of rev cell injury
- results from malfunction of Na-K pumps (Na ions flow into cells…H2O follows–>
- generalized swelling in cells of whichever organ is effected; megaly: increase in size/weight; ie: splenomegaly during mono
Intracellular accumulations
(reversible cell injury)
could happen from genetic disorder or enzymes missing..
1 excessive amts of normal intracell substances (ie proteins, lipids, carbs etc)
2 accum of abnormal sub pro by cell bc of issues (cellular stress–>accumulation of (abnormal) broken down proteins)
3 accumulation of pigments and particles that cell is unable to degrade (ie newborns w imm liver & increased RBC (which the liver can’t process)–> accumulation of bilirubin–> discoloration of skin
Cellular adaptions: responses to increase/decrease in functional demand…
atrophy: cells shrink and reduce their differentiated function; protective mechanism for E conservation, but negative if goes on too long; ie: during ischemia, starvation, differences w/ endocrine processes
hypertrophy: increase in cell size accompanied by augmented functional capacity (bc working harder); ie cells that can’t reproduce and undergo mitotic div would hypertrophy
hyperplasia: increase in # of cells by mitotic division
* can have hypertrophy/plasia at same time, ie pregnancy- breast tissue undergoes both; ie: hypertension
cellular adaptions: responses to persistent injury
metaplasia: replacement of one differentiated cell type w/ another; ie: smokers w/ chronic irritation of bronchia mucosa–> change of cells to handle the stress
dysplasia: disorganized appearance of cells bc of abnormal variations in size, shape and arrangement
* HPV can have either - hopefully doc intervenes at metaplasia, before dysplasia can begin
* either can lead to cancerous cells
Irreversible cell injury
Necrosis & apoptosis
- both are processes that lead to cell death
- could have both together in same process (heart attack)
necrosis
- consequence of external injury or ischemia (inadequate blood supply to an organ or part of the body, especially the heart muscles)
- characterized by cell rupture caused by disruption of plasma/cell membrane–> intracell contents spill out–> inflammation;
- take lab values of spillage to monitor the prob
apoptosis
- can happen as natural progression of cell life or if signals sent
- no breaking of membrane/spillage/inflammation
- “organized cell death”
- norm process
ie dementia pt - change in CT scan shows atrophy of brain related to apoptosis
nutritional cell injuries
deficiencies (ie iron, vit D)
&
excess (ie Na excess = hypertension; fat excess = obesity…diabetes)
chemical cell injuries
free radicals heavy metals (ie lead) toxic gases (ie CO2 poisoning)
Physical & Mechanical cellular injuries
- temp extremes: too hot, heat stroke; too cold, frost bite
- abrupt changes in atmospheric pressure: altitude increase can lead to cell injury if they don’t adapt; altitude decrease and lead to N imbalance “the bends
- abrasion…trauma
- electrical: ie burns
- radiation: can cause damage…1 directly to DNA; 2 creates free radicals –> cell dysfunction–>necrosis
Infectious & Immunologic cellular injuries
~Bacteria:
- endotoxins: toxins inside bacteria released when bacteria killed (plasma wall broken)–> wreaks havoc on body
- exotoxins: released/excreted by bacteria as a protective mechanism to stay alive (ie cholera/dyptheria)
~Virus: invades cell and replicates
~Indirect immunologic responses too
Rel bw host and pathogen:
symbiosis, mutualism, and commensialism
benefit human/no harm to microorganisms
benefit to both
benefit microorganisms/no harm to human
pathogenicity
benefits organism/harms human; ability of microorganisms to cause disease
toxigenicity
ability of microbe to produce endo/exo toxins; thought to be more virulent
immunogenicity
ability of pathogen to induce immune response (toxins, enzymes, mobility etc)
virulence
how severe of a disease a mircroorg may cause
endo v exo toxins
endo: toxins inside that are released when cell wall ruptured (organism is killed)
exo: toxins excreted by org (ie: tetanus)
bacteria
single cell; rigid wall; no internal organelles
cocci/bacilli/spiral
gram +, -, acid fast (resist stain)
aerobic or anaerobic
fungi
eukaryotic; w/ organelles- complex structure; rigid wall; often part of normal flora, but cause prob when body’s defense compromised (ie: mycotic infection); located superficial/cutaneous, subcutaneous (ulcer/abcess), and systemic
parasites
best themselves w/ host and live off of/benefit from them; protozoa (single cell); helminths (round/flat worms); arthropods (lice/ticks); **most often on skin/in GI tract
viruses
most common affliction;
simple microorg-no metabolism and can’t reproduce independently; must infect host to replicate
hard to treat/prevent bc of ability to adapt
can bypass defense mech bc they dev intracellularly (which gives them protection)
incubation stage
period from initial exposure to onset of 1st symptoms; contagious before you knew you had it
prodromal
occurrent of initial symptoms (mild)
illness
pathogen multiplies rapidly; immune/inflamm responses triggered; dev symptoms specific to pathogen
convalescence
1- immune/inflamm systems have successfully removed agent and symptoms go down
2- latent phase w/ resolution until reactivation
3- fatal
subclinical
pt functions normally even tho disease processes are well established (subclinical hypertension)
clinical manifestation of infection
use for assessment of patient
*majority of s/s from inflammation
nonspecific s/s: fatigue, malaise, weak, aching, decreased app
hallmark s/s is fever, except for older pt and immunosuppressed pt
aplastic anemia
bone marrow suppression leads to decreased production of RBC (toxic, radiation, immune injury)
anemia of chronic disease
chronic infection, inflammation, malignancy leads to increased demand or suppression of RBC
folate deficiency (B vit)
lack of folate leads to premature cell death
Iron deficiency
most common cause of anemia and most common nut deficiency in the world
lack of iron leads to lack of hemoglobin
thalassemia
impaired synthesis of hemoglobin chain; congenital
sickle cell anemia
abnormal hemoglobin molecule (don’t have same o2 carrying ability); congenital
hemolytic disease of newborn
maternal antibodies cause destruction of fetal cells
acute blood loss
as related to type of anemia
blood loss leads to insufficient RBC
pernicious anemia
lack of vit B leads to altered DNA synth
post hemorrhage (as related to type of anemia)
blood loss leads to insufficient RBC
erythropoiesis
hormone secreted by kidney in response to cellular hypoxia; stimulates RBC production in bone marrow
claudication
pain in muscle
DPG
type of salt in cell’s protein- helps hgb release o2 easier (more DPG = more o2)
cardiac output
volume of blood output from heart per min; made up of two components: CO = HR x SV
Stroke volume (SV)
volume of blood pumped out of the left ventricle with every heart beat
mild symptoms of anemia
none; compensatory mechanisms are working
moderate symptoms of anemia
fatigue, malaise, loss of E, tachycardia, exertional dyspnea
mod to severe symptoms of anemia
orthostatic/general hypotension; vasoconstriction->pallor; tachypnea/dyspnea; tachycardia/transient murmur, angina pectoris; intermittent claudication; night cramps in muscles; h/a, light headedness, faintness; tinnitus (noise/ringing in ears)
relative v absolute anemia
relative: increase in total RBC mass with an increase in plasma vol (which causes decreased hgb content in bl…diluted); ie: pregnancy
absolute: decrease in number of RBC
microcytic anemia
type of iron def anemia (secondary to…); presence of hypochromic RBC in bl smear
Hypochromic anemia
generic term for any type of anemia in which the RBC are paler than normal. (Hypo- less, chromic-color.) A normal red blood cell will have an area of pallor in the center of it
etiology of iron deficiency anemia
1 decreased absorption (bc of body’s ability/chronic illness)
2 physiologic increase in general requirement (pregnancy)
3 excessive iron loss (normal bl loss)
4 renal issues
hemostasis
physical process that stops bleeding @ site of injury while maintaining norm bl flow elsewhere
primary hemostasis
interaction between platelets and the endothelium of the injured blood vessel; immediate response to trauma is vasoconstriction to reduce blood loss, resulting from vasospasm; then forms “platelet plug” that adheres and clumps in 3-7m
secondary hemostasis
involves formation of fibrin clot (coagulation) to maintain primary hemostasis efforts; happens via intrinsic/extrinsic pathways and is series of clotting factors being activated (fibrinogen to fibrin) over 3-10m; final stage: clot retraction (firm clot formed) by 1h
key players in hemostasis
always in body; part of both primary and 2ndary hemostasis
- platelets (thrombocytes): activators coagulation factors; degranulation triggers the cascade effect; stickiness helps them adhere to endothelium and each other (clump together)
- coagulation factors: activated by platelets, and then activate each other or tissue factors; mostly plasma proteins produced by the liver that are normally circulating in the blood
prothrombin (PTR) & INR lab tests
evaluate extrinsic pathway of coagulation
activated partial thromboplastin time (aPTI) lab test
evaluate intrinsic pathway of coagulation
Virchow’s triad
(risks for thrombus)
- circulatory stasis: (immobile/laying for period of time)
- hypercoaguable condition: body pushed towards increased coagulation ie: pregnancy, oral contra, chemo/cancer pt, obesity
- endothelial/vessel wall injury: trauma ie: IV, cath, smoking, hypertension
- *C-s pt meets all these criteria!
blood pressure equation
BP = CO (bl vol output/min) x SVR (resistance overcome to push bl thru circ system & create flow)
edema/hypervolemia
excessive accumulation of fluid w/in the interstitial space
forces involved in edema/hypervolemia
1 increased capillary hydrostatic pressure
2 increased interstitial oncotic pressure
3 increased cap membrane permeability
4 lymphatic channel obstruction (can’t carry waste away)
clinical dehydration/hypovolemia
too small volume of fluid in the extracellular space (vascular/plasma/interstitial); body fluids are too concentrated
forces involved in dehydration/hypovolemia
1 fluid loss: emesis, hemorrhage, diarrhea, polyuria, diaphoresis
2 reduced fluid intake: GI issues/altered mental status
3 fluid shift: burns…edema in some spaces but not the right ones (interstitial space)
Na
135-145 mEq/L major ECF cation nerve conduction & neuromuscular fct regulates acid-base balance maintains water balance
clinical manifestations of hyponatremia
CNS dysfunction:
confusion/lethargy…seizures/coma
n/v, h/a
clinical manifestations of hypernatremia
(increased conc of fluid = dehydration)... thirst/dry mucuous membranes hypotension tachycardia oliguria confusion/lethargy...seizures/coma
Potassium
3.5-5 mEq/L major ICF cation cardiac muscle contractions maintains acid-base balance neuromuscular transm of nerve impulses *heart and GI
clinical manifestations of hypokalemia
- smooth and skeletal muscles HYPERpolarized (less reactive to stimuli); ie: GI- abdominal dissension, decreased bowels/paralytic ileum; general muscle weakness
- cardiac: dysrhythmias
clinical manifestations of hyperkalemia
- smooth and skeletal muscles HYPOpolarized- can’t fire again after discharge; GI cramping/diarrhea; general muscle weakness
- cardiac: dysrhythmias/cardiac arrest
- dialysis if kidneys not functioning
Calcium
9-11 mg; 4.5-5.5 mEq/L heart protectant- cardiac AP CNS- nerve impulse transm bone, teeth, muscle contraction blood coagulation
clinical manifestations of hypocalcemia
increased neuromuscular excitabilit/hyperactive reflexes: twitching, seizures, tetany
heart dysrhythmias
clinical manifestations of hypercalcemia
decreased neuromuscular excitability/diminished reflexes: weakness, paralysis, constipation
CNS: fatigue, lethargy, confusion
n/v
heart dysrhythmias- heart block, bradycardia
kidney stones
3 major mechanisms regulating acid-base status
Bicarbonate-carbonic acid buffer system (ECF; always happening in body); 20 HCO3: 1 CO2; *body adjusts carbonic acid to maintain pH ratio respiratory system (2nd line- fast acting) renal system (2nd line- slow acting)
respiratory acidosis
condition that causes excess carbonic acid (aka you’re shallow breathing/not taking deep breaths)…
- impaired gas exchange: asthma, COPD, pneumonia
- inadequate neuromuscular fct: injury, surgery, pain
- impairment of respiratory control in the brainstem: opioids
ABG’s: increased co2 and decreased pH
clinical manifestations of respiratory acidosis
neuro: blurred vision, tremors
h/a, lethargy
tachycardia, heart dysrhythmias
respiratory alkalosis
condition that causes a carbonic acid deficit: hyperventilation– panic attack, anxiety, crying (peds), acute pain, hypoxemia, brain stem injury
ABG’s: decreased CO2 and increased pH
clinical manifestations of respiratory alkalosis
increased neuromuscular excitability- numbness, tingling, spasms
excitation/confusion
cerebral vasoconstriction
Metabolic acidosis
excess of any acid except carbonic acid
- increase in metabolic acid (diabetic ketoacidosis (type I), burns, shock
- decrease in base (bicarb): severe diarrhea, intestinal decompression
- combo of both
ABG’s: decreased HCO3 and decreased pH
clinical manifestations of metabolic acidosis
fruity breath
GI: n/v, diarrhea–>dehydration
CNS dep: h/a, confusion, lethargy, coma
cardiac: tachycardia, dysrhythmia
metabolic alkalosis
deficit of any acid except carbonic acid
- increase in base: overuse antacids, hypovolemic
- decrease in acid: emesis, gastric secretion removal (tube)
- combo of both (hypokalemia…diuretics)
ABG’s: increase in HCO3 and increase in pH
clinical manifestations of metabolic alkalosis
CNS irritability, and then depression: tingling, tetany, seizures
ECF vol depletion: n/v, diarrhea, hypotension
hypokalemia w/ muscle weakness
bacterial enzyme
helps organism exist in environment
antiphagocytic factors
microbes containing outside coding that leave them unrecognizable to body’s phagocytic defense mechanisms (leukocytes)
also help w/ adherence
mode of transmission
droplet, airborne, oral/fecal, vector
vector
any get that carries/transmits an infectious pathogen into another living organism
negative intraplural pressure
produced by babies (coughing/crying) to open collapsed alveoli after birth
importance of surfactant
decreases the surface tension of alveolar fluids and helps alveoli open more easily after birth
reasons of closure for…
foramen ovale
ductus arteriosus
ductus venosus
- pressure change in atria
- increased oxygen of blood
- unsure
-plasia
growth & dev (mitotic division)
ie: increased altitude–> body produces more RBC
mechanism of lack of o2 in body
atp pro in cell ceases ATP dependent pumps fail Na accumulates in cell-> cell swells excess calcium interferes glycogen depleted lactic acid produced pH decreases...causes dysfunction
reperfusion injury
- calcium overload (when we reperfuse body is washed w ca
- formation of reactive o species
- *both can trigger apoptosis
- inflammation
mycoses/mycotic infection
any disease/infection caused by fungi
chain of infection
agent resevoir portal of entry/exit mode of trans portal of exit/entry host
pica
craving of non-food substances; can occur w/ iron deficiency anemia
vascular purpura
disease causing swelling/inflammation of bl vessels (vasculitis)
when bl vessels bleed you get the purpura rash
normal platelet count
200k-400k
<100k? hemorrhage concern…bl can’t clot…can’t admin pitocin
types of coagulation disorders
deficiencies of one or more clotting factors
- vit k def…admin supp
- inherited: Von Willebrand- lack of glycoprotein in bl, causing inability to clot; hemophelia- bl can’t clot normally
- disseminated intravascular coagulation (DIC)- late stage of HELLP
hemarthrosis
blood in joints
hematoma
blood in brain
petechia
capillary hemorrhages;
*purpura are groups/patches of peticha
hemtochezia
blood in stool
hemoprysis
blood in sputum
intrinsic v extrinsic pathway of coag cascade
intrinsic is triggered when bl comes into contact w/ endothelium…platelets forming
extrinsic triggered by tissue factor (trauma)
*both pathways come down to common pathway and activate factor X….which activates Xa
treatment of bleeding discorders
- avoid cause (from a med? stop the med!)
- steroids- stimulates immune response- prevents breakdown of platelets
- admin IVIG - intravenous immunoglobulin…prevents bleeding (in the short term - days/weeks)
- factor replacement (whichever needed)
- admin plasma/platelet
thrombocytopenia
decreased pro or increased demand of platelets
assess: petechiae, purpura, bleeding, decreased platelet count in lab
treat: treat/remove root of cause; block imm response; bl/platelet transfusion
deep vein thrombosis
i. d.: ultrasound or labs->d dimer (neg= don’t have)
treat: thrombolytic (tPA) med to break down clot; anticoagulant to prevent further clotting
estrogen (as related to UTI)
the urethra is an estrogen dependent structure; lack of estrogen = more prone to infection; lack of estrogen–> prepubescent/post menopause
uropathogenic properties (pathogens causing UTIs)
- ability to attach to uroepithelial cells (fimbriae/pilli)
- ability to attach to latex cath
- ability to express toxins
- ability to produce biofilms (harder to breakdown/eradicate)
most common uropathogens
e coli STIs pseudomonas staph sprophyticus klebisella proteus
PID
infection of cervix (cervicitis), ovaries (oophoritis), uterus (endometritis), oviducts (salpingitis)
aerobic & anaerobic
gonorrhea and chlamydia most common
mechanisms behind preeclampsia
maternal immunologic intolerance
abnormal placental implantation
CV/inflamm changes
labs to draw for hypertensive disease in pregnancy
protein in urine
liver enzymes
platelet count (low= thrombocytopenia–>hemorrhage)
