Patho Exam 1 Flashcards
Components of the hematologic system
bone marrow, blood (RBC, WBC, platelets), spleen, and lymphatics
plasma vs serum
serum is plasma minus clotting factors (fibrin/fibrinogen)
Main plasma proteins
albumin, clotting factors (fibrinogen), and globulins (alpha, beta, and gamma)
Formed elements of blood (and rough #s)
Platelets(250-400 thousand), erythrocytes (4.2-5.8 million), leukocytes (5-9 thousand)
normocytic, microcytic, macrocytic
normal size, small size, large size
normochromic, hypochromic, hyperchromic
normal color, pale color, vivid color
average life span of RBCs
120 days
what removes old RBCs from the bloodstream?
reticuloendothelial cells in the liver and spleen
what happens to hemoglobin when RBCs are destroyed?
some is recycled and some is broken down to form bilirubin and secreted in bile
what happens to iron when RBCs are destroyed?
it is recycled to form new hemoglobin molecules in the bone marrow
Normal levels hemoglobin in men, women
M: 13-18 g/100mL; W: 12-16 g/ 100mL
Normal hematocrit levels men, women
M: 37-49%; W: 36-46%
what is the mean corpuscular volume (MCV)?
The average size of individual RBCs
Normal RBC count in men, women
M: 4.5-5.3 million/mm3; W: 4.1-5.1 million/mm3
what is hematocrit?
% of RBCs in the plasma
what is hemoglobin?
Oxygen-carrying compound composed of a pigment (heme), which contains iron, and a protein (globin)
What does a decrease in plasma volume do to a person’s hematocrit level?
increases it–decrease in plasma volume causes increase in hematocrit.
Would dehydration cause increase or decrease in hematocrit?
Increase–loss of plasma volume would increase hematocrit
Increase or decrease hematocrit?
- decrease plasma volume
- deydration
- overhydration
- decrease # RBCs?
- increase
- increase
- decrease
- decrease
Hematocrit is helpful for assessing magnitude of what?
blood loss
If hematocrit is drawn immediately after blood loss, what will the results show? What about over time after loss?
Normal levels. RBCs and plasma lost in equal proportions. Over time the body will compensate for loss by shifting fluid from interstitial space into bloodstream, so the hematocrit will go down (RBCs will be less % of blood…can’t make them as quickly as can shift fluid from interstitial space into bloodstream)
What causes a decrease in hbg (hemoglobin)?
blood loss, hemolytic anemia, bone marrow suppression.
If a patient has a normal RBC level but low hbg, what does this indicate?
iron deficiency anemia
What are leukocytes?
Granulocyte (neutrophils, eosinophils, basophils), agranulocyte (T/B cell lymphocytes, monocytes, tissue macrophages), and platelets
what is erythropoiesis?
the production of red blood cells
What triggers erythropoiesis?
Low oxygen levels trigger the kidneys to produce erythropoietin (hormone), which stimulates myeloid stem cells in bone marrow to make red blood cells
What nutrients are required for erythropoiesis?
iron, B12, folate, B6, protein, other factors
A decrease in the levels of iron, B12, folate, B6, protein, or other factors would lead to..?
decrease in production of RBCs, anemia.
What impact does iron deficiency have on RBCs?
results in small RBCs, less iron would impact hemoglobin and ability to carry O2
What causes the formation/production of megaloblasts and what are they?
Vitamin B12 and folate deficiency. Abnormally large RBCs/erythrocytes.
What role do B12 and folate have in erythropoiesis? How doe people get these nutrients?
They;re required for the synthesis of DNA in RBCs. Derived from diet (except in vegetarians–b12 only in animal origin foods)
where does erythropoiesis occur?
bone marrow
what stem cells form erythrocytes?
hemocytoblasts
erythroblasts, erythrocytes….nucleus?
erythroblasts have nucleus, erythrocytes do not.
what is erythropoietin?
hormone produced at kidneys in response to low O2, primary regulator or erythropoiesis
what is anemia?
lack of adequate #s of mature, healthy RBCs resulting in inefficient O2 carrying capacity/delivery to cells/tissues
what is a reticulocyte? What does it mean if you have increased levels of them?
immature red blood cells. If increased # of reticulocytes, it indicates that the body is trying to compensate for anemia,
What are some indicators of anemia?
Low hbg and hct, low RBC count, increased reticulocyte count
What are some signs and symptoms of anemia?
Fatigue, SOB that worsens with exertion, dizziness, cold intolerance
How do you assess for anemia?
pallor, tachypnea, tachycardia, cold extremities, labs (RBC count, hct, hbg, reticulocyte count)
Difference between anemia with acute vs chronic blood loss
both: low hct, hbg, low RBC count
acute: high reticulocyte count
chronic: low iron-can’t recycle
most common cause of anemia? how does it work?
iron deficiency anemia. Iron is essential for the formation of heme, the part of Hgb responsible for attaching oxygen for transport. Normal erythropoiesis cannot occur
aplastic anemia
suppression of bone marrow production of RBCs.
most common hemoglobinopathy & inheritance
sickle cell anemia. autosomal recessive
thalassemia & inheritance
abnormal hbg (alpha or beta) and large amounts of RBC formed leads to deformities, weak bones. autosomal recessive.
polycythemia
excess RBCs > thick blood > increase peripheral resistance dec. blood flow > inc. clotting
WBCs include…
granulocytes and agranulocytes
granulocytes
neutrophils (mature = segmented, immature = banded) , basophils, eosinophils
agranulocytes
lymphocytes (B and T cells) and monocytes (macrophages)
less mature neutrophil called ________ and an increase in these indicates…
band cell…body is trying to fight off infection (shift to left = increase in immature neutrophils)
function of monocytes; where located?
transform into macrophages to remove debris and phagocytize bacteria@ tissues. particularly @ spleen, liver, peritoneum, alveoli.
Lymphocytes
T and B cells
normal range for total WBC count?
4500-11000/mm3
neutrophilia
increase in neutrophils and bands. often indicative of infection.
neutropenia
decrease in neutrophils and agranulocytosis (dramatic decrease in granulocytes. ANC critical @
thrombocytes
platelets
platelets form from _____ by _____
megakaryocytes by endomitosis. instead of producing daughter cells, fragments into pieces.
how long do platelets last in the bloodstream?
~10 days
what’s the function of platelets?
blood clotting/ coagulation/ control bleeding
describe the clotting cascade…
platelets adhere to injury site > extrinsic and intrinsic pathways activated to release factor X (both pathways) > prothrombin > thrombin > fibrinogen to fibrin
blood is ~____% water
90%
where is albumin produced?
liver
plasma minus fibrinogen/clotting factors
serum
hemostasis
blood clotting (stopping of blood)
under normal (not injured) conditions, endothelial cells secrete prostacyclin, nitric oxide, CD39 enzyme, which do…
prostacyclin = prostaglandin
NO = vasodilator, inhibit platelet aggregation
CD39 enzyme = breaks down ADP in blood. OVERALL: assure platelets don’t stick together or to vessel wall
vWf (von Willibrand factor)
produced by endothelial cells, helps to bind collagen and platelets together when vessel injured
blood clot consists of…
fibrin, platelets, and trapped RBCs
prothrombin time (PT)
amount of time it takes liquid portion of your blood to clot. evaluates extrinsic pathway of coagulation cascade. normal = 11 to 13.5 sec
INR
international normalized ration. normal = 0.8-1.1. Above normal = blood clotting too slowly. If on blood thinners, INR 2-3. More than 3
what does D-dimer measure?
fibrin degradation products. indicates recent clotting activity.
substances primarily responsible for decreasing/dissolving clots?
Plasmin, plasminogen, tissue plasminogen activator (tPA)
fibrinogen levels indicate…
reflect clotting activity/ability. may be elevated with inflammation, infection
aPTT
measures time to clot. evaluates intrinsic coagulation cascade.
platelet aggregation
evaluates platelet ability to adhere, form clumps. If abnormal, bleeding risk
ITP, TTP, vWD, DIC
clotting disorders
types of immunity
natural (nonspecific, 1st line), acquired (develops with exposure-humoral (B) or cellular (T))
humoral immunity
B cells detect specific antigen and produce antibodies/immunoglobilins. 2nd line defense. Operates @ humor/blood.
cellular immunity
T lymphocytes detect antigen and transform into cytotoxic T cells to “kill” infected cells. Operates @ cellular level
B cells differentiate into
effector cells (produce antibodies) and memory cells ( remember antigens/MHCs for faster response next time)
when cell detects foreign body/pathogen, what’s the next step?
Forms MHC/APC and presents “flag” on surface for B (@ blood) or T(@cell) cells to recognize/respond to
leukocytes vs. lymphocytes
leukocytes (neutrophils, eosinophils, basophils, monocytes, macrophages) and lymphocytes (B, T, and NK cells)
where do immune cells originate? mature?
all immune cells originate @ bone marrow. B cells mature @ bone marrow, T cells mature @ thymus.
immune system @ skin
1st line defense. antimicrobial proteins and protection.
immune system @ bone marrow
immune cells all produced at bone marrow
immune system @ bloodstream
immune cells circulate through blood stream looking for pathogens/infected cells
immune system @ thymus
T cells mature @ thymus
immune system @ lymphatic system
immune cells converge @ lymph nodes. travel/comm of immune cells @ lymphatic system.
immune system @ spleen
immune cells enriched @ certain parts of spleen
immune system @ mucosal tissue
prime entry points for pathogens > specialized immune hubs (Peyer’s patches where immune cells “sample” GI tract)
4 stages of immunity
recognition, proliferation (of B/T cells), response (Ab or cytotoxic Ts), effector (immune cells begin to destroy pathogens)
How to antibodies/immunoglobulins work to destroy pathogens?
agglutination (clumping), opsonization (coat with sticky substance), histamine production, activate complement system
IgG
most common. blood borne and tissue infections. activates complement system.
IgA
body fluids. protects against respiratory, GI, and GU infections
IgM
intravascular serum. 1st in bacterial infections.
IgE
in serum. allergies. combats parasitic infections.
IgD
role unknown.
types of T cells and roles
Effector (activate when find antigen, attract other cells–B,Tc, NK, macrophages), cytotoxic T (attack cell w/ cell lysis & cytolytic enzymes), suppressor T (feedback loop. check B cell production), memory T (rec. from earlier exposure)
complement system
circulating plasma proteins help fight off invading pathogens (vessel size, permeability, clotting, enhance chemotaxis). Promotes inflammatory response.
CBC count
complete blood cell count (leukopenia v. leukocytosis & WBC differential)
normal leukocyte levels (adult)
7400/uL
leukemias
problematic B/T stem cell formation @ bone marrow.
Characteristic sign of non-hodgkins lymphoma
lymphademopathy (enlarged lymph nodes)
pathophysiology
biological and physical manifestations of disease and associated functional changes.
health
state of complete physical, mental, and social wellbeing, not just absence of disease
homeostasis
“steady state” maintenance . constantly changing to regulate and keep body at optimal levels of functioning
constancy
never changing
stress
challenge, threat, damage to a person’s equilibrium. a state manifested by a specific syndrome of the body developed in response to any stimuli that made an intense systemic demand on it
adaptation / resilience
an individual’s unique capacity to adapt to or cope with the stressor
types of stressors
physical (cold, heat), physiologic (pain, fatigue), psychosocial (isolation, fear)
stress response 3 stages
alarm, resistance, exhaustion
alarm stage of stress response
HPA axis, fight or flight response. defensive, anti-inflammatory. limited.
resistance stage of stress response
adaptation to stressor. cortisol still increased.
exhaustion stage of stress response
endocrine activity increases. negative consequences of long term stressors.
Psychoneuroimmunology
Study of the interactions between our mind (consciousness, brain, and CNS) and immune function
what does cortisol do to immune response
suppresses inflammatory response. relationship between stress and sickness because can’t fight off infections as well w. high cortisol levels
sympathetic nervous system (SNS)
fight or flight response. epic/norepi released > shuts blood to vital areas, increases BP (in trauma, trying to return BP to normal when hypotensive/hypovolemic shock/ etc.)
RAAS pathway
drop bp/bvol > kidneys release renin/angiotensin > inc. angiotensin I (kidney), II > angiotensin II (lung) stimulates vasoconstriction to inc. bp and > stimulates adrenal cortex to release aldosterone > increases reabsorption of H2O, Na > inc. blood volume > BP to normal
cortisol release
Hypothalamus - CRH (corticotropin-releasing hormone) > ant. pituitary - ACTH > adrenal cortex - cortisol
angiotensin II f’n
promotes vasoconstriction
aldosterone f’n
promotes reabsorption of water, sodium. released @ adrenal cortex
cortisol f’n
alters glucose, fat, protein metabolism (from storage to supplying…increase blood glucose); suppresses inflammatory and immunes response. Aid fight or flight response.
antidiuretic hormone (ADH) & how works
vasopressin. causes vasoconstriction. Stimulates kidneys to reabsorb water from urine to blood.
cortisol @ chronic stress, PTSD
cortisol elevated with chronic stress, decreased with PTSD
Chronic stress and neuroendocrine and metabolic stress…
chronic stress >elevated cortisol/epi/norepi levels > insulin resistance > inc. blood glucose > link with inactivity and overeating
positive and negative feedback loop
positive promotes more of activity (i.e. clotting) and negative stops activity (i.e. blood pressure return to normal w/ RAAS)
hypertrophy
enlarged muscle mass that happens with increased workload
atrophy
loss of muscle mass associated with loss of use, disease, dec. blood/ nerve supply, etc.
hyperplasia, dysplasia, metaplasia
hyper = increase in # new cells dys = abnormal cell changes meta = change of cells to unusual former tissue where it's found
cellular injury and common causes
disruption of steady state regulation. commonly caused by hypoxia, nutritional imbalances, physical agents, chemical injury, infectious agents
inflammation and purposes
innate, automatic response to neutralize harmful agents, remove dead tissue, generate new growth, promote healing
inflammatory response
injury > chemical signals like histamine released > increase vascular permeability > more fluids, WBC to injury site > WBCs “eat” pathogens, debris > tissue heals
gene
sequence of DNA that contains instructions for making RNA molecules/proteins.
transcription
DNA to RNA
translation
RNA to proteins
induction
turn gene “on”
repression
turn gene “off”
genotype
genetic makeup/material
phenotype
expression of genetic makeup/physical characteristics
polygenic
many genes affect one trait
allele
copy of a gene. if alike, homozygous. if different, heterozygous. if only have one copy, homozygous
interstitial fluid
A filtrate of the blood; located between cells and between cells and capillaries. contains water, sodium
diffusion
passive transport of molecules from high conc to low conc
osmosis
movement of water from less conc sol to more conc sol. Movement of WATER.
facilitated transport
The passing of certain molecules through the plasma membrane with assistance from carrier proteins. i.e. glucose with carrier insulin
active transport
requires energy. goes against concentration gradient. sodium potassium pump powers movement.
sodium is more prevalent in/outside cells?
outside
potassium is more prevalent in/outside cells?
inside
normal sodium level
140 mEq
normal potassium level
5 mEq
hydrostatic pressure
force exerted by water in bloodstream. source: heart pumping.
osmotic pressure
pressure exerted by solutes (i.e. electrolytes) in solution (bloodstream)
Oncotic pressure
force exerted by albumin (plasma protein) in bloodstream.
normal serum albumin
3.1-4.3 g/ dL
total albumin levels indicate…
overal nutritional level of pt.
Osmolality + normal levels
if take solutes out of solution and measure their mass per kg of solvent. Based on 1 mole (6.02 * 10^23). Normal = 282-295mOsmoles / kg water.
Osmolarity
Osmoles per L of solute (R in osmolarity and liter). Mainly sodium. Found in extracellular space.
What is osmolality used for in clinical practice?
determining hydration status
Isotonic
same tonicity as blood; does not cause fluid shifts or alter body cell size
Hypotonic
fewer particles and more water than blood and body fluids. Adds water to the bloodstream and causes a fluid shift from ECF to ICF, causing cells to swell.
Hypertonic
contains more particles and less water than blood and body fluids. Adds solutes to the bloodstream and causes fluids to shift from ICF to ECF, causing body cells to shrink
fluid output @ kidneys
1 mL urine/Kg/hr.
fluid loss @ skin
perspiration, evaporation
fluid output @ lungs
300mL/ day
fluid output @ GI
100-200 mL/ day
most significant factor in urine concentration
presence/absence of of ADH
Natriuretic peptides
Three major peptides that promote natriuresis (excretion of large volumes of both sodium and water by the kidneys in response to excess ECF volume). Atrial natriuretic peptide (ANP), Brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP)
hypovolemia
dehydration
hypervolemia
overhydration
Hypo/pernatremia
too little/much salt
Hypo/perkalemia
Too little/much potassium
hypo/percalcemia
too little/much calcium
hypo/perphosphatemia
too litte/much phosphate
hypo/permagensemia
too little/much magnesium
s/s, assessment, tx, testing for hypovolemia
s/s: thirst, dry membranes, weakness
assessment: little, dark urine, turgor poor, hypotension, dry membranes
tx: oral fluids
testing: blood urea nitrogen elevated, oliguria (abn. small amt urine), hypernatremia
s/s, assessment, tx, testing for hypervolemia
s/s: edema, weight gain
ass: SOB/fluid, crackles, edema/pitting, weight
tx: Diuretic
test: dilutional hypernatremia
s/s, assessment, tx, testing for hyponatremia
s/s: muscle cramps, weakness, headache, confusion
ass: weakness, depression, anxiety, lethargy, confusion
tx: depends on cause
test: Serum sodium levels
extracellular electrolytes
Na, Cl
intracellular electrolytes
K, Mg, PO4,
Sodium reference range
136-145 mEq/ L
potassium reference range
3.5-5.1 mEq/ L
calcium reference range
9-10.5 mg/ dL
bicarbonate reference range
21-30 mEq/ L
s/s, assessment, tx, testing for hypernatremia
s/s: dec. saliva, thirst, headache, agitation, seizures
ass: turgor, reflexes, tachycardia, thready pulse, vol. changes
tx: replace water if necessary
test: serum sodium >145 mEq/ L
s/s, assessment, tx, testing for hypokalemia
too little potassium.
s/s: anorexia, nausea, vomiting, weakness/cramping
ass: postural hypotension, muscle weakness
tx: oral, parenteral K+
test: serum pot
s/s, assessment, tx, testing for hypokalemia
too little potassium.
s/s: anorexia, nausea, vomiting, weakness/cramping
ass: postural hypotension, muscle weakness
tx: oral, parenteral K+
test: serum pot
IV potassium: yay or nay? why?
nay. potassium is extremely caustic to veins, careful about infiltration. can also cause fatal dysrhythmias b/c affects muscle function. lethal injections. in emergencies can be given DILUTED via CENTRAL LINE.
s/s, assessment, tx, testing for hyperkalemia
too much potassium s/s: nausea, cramping, diarrhea, muscle weakness/cramping ass: muscle weakness, cramping tx: dextrose, insulin, sodium bicarb test: serum potassium levels
s/s, assessment, tx, testing for hypocalcemia
s/s: tetany, laryngeal spasm, bone pain, fx, confusion, seizures
ass: tetany, hyperactive reflexes, Chvostek/Trousseau’s signs, hypotension
tx: admin Ca2+ and Vit D.
test: serum calcium level
tetany
body-wide cramping
Chvostek signs
tap facial nerve > induce lip twitches to facial spasms
Trousseau’s sign
inflate BP cuff > occlude arterial BP 3-5 min > induces carpopedal spasm
s/s, assessment, tx, testing for hypercalcemia
s/s: anorexia, nausea, constipation, muscle weakness, bone fx
ass: dec. muscle excitability, ataxia, loss muscle tone
tx: fluids, loop diuretics, biphosphonates, calcitonin, dialysis
test: serum calcium > 10.5 mg/ dL
s/s, assessment, tx, testing for hypophosphatemia
s/s: tremor, lack coordination, confusion, joint stiffness
ass: tremor, ataxia, weakness, dec. refelxes
tx: replace PO4-
test: serum phosphorous level
s/s, assessment, tx, testing for hypomagnesemia
s/s: cramps, muscle change, uncontrol mvmt
ass: + Chvostek/Trousseau, Babkinski, nystagmus, htn
tx: replace Mg2+ therapy
test: serum magnesium
Babinski signs
toes fan out with “tickle” bottom of foot
s/s, assessment, tx, testing for hypermagnesemia
s/s: lethary, confusion, weakness
ass: hyporeflexia, hypotension, weakness
tx: IV calcium or dialysis
test: serum magnesium level >2.5 mg/dL, arrhythmia
acid
donates H+, pH
base
accepts H+, pH > 7.0
carbonic acid link
H2CO3 links respiratory and metabolic systems. @ lungs regulate by changing breathing rate/depth. @ kidneys regulate by absorbing/excreting acids/bases
partial pressure of CO2 (PCO2)
35-45 mmHg
describe respiratory compensation (pH)
receptors @ arteries sense changes in PCO2, if too low (resp alkalosis), stimulate respiratory center @ medulla to inc. breathing rate. if too high (resp acidosis), decrease rate. Compensation only moderately effective, but fast.
describe metabolic compensation (pH)
kidneys control pH by regulating level of bicarb(HCO3-) reabsorption and H+ reabsorption or excretion. Slow compensation. Takes days to reach max effect.
respiratory alkalosis
too much CO2 is blown off, blood become alkaline (hyperventilation)
ABGs (arterial blood gasses)
measure blood acidity, partial pressure of O2 &CO2, O2CT & O2Sat, and HCO3-
pH reference values (arterial)
7.35-7.45 pH
PaCO2 reference values (arterial)
35-45 mmHg
acidemia
pH > 7.45. 7.8+ can be fatal
alkalemia
pH
PaO2 reference range
80-100 mmHg
PaO2
hypoxemia
hyperventilation/hypocapnia
PaCO2
hypoventilation/hypercapnia
PaCO2 > 45 mmHg. Hypercapnia = too much CO2 in blood. Results from breathing too low/shallow, don’t blow off enough CO2.
what % of O2 carried by hbg molecules?
97%
normal O2Sat
95-98%
normal O2Sat (SaO2)
95-98%
bicarbonate (HCO3-) reference range
21-28 mmol/L
metabolic acidosis
> 26 mEq/L HCO3-
metabolic alkalosis
buffer ions
bicarbonate, phosphates, hbg, plasma proteins
Low PO2
hypoxia, hypoemia
elevated PCO2
hypercapnia
low PCO2
hypocapnia
Interpreting ABGs
- pH (acid or alkalosis)
2. PCO2 (PCO2 > 45 hypovent,
