Pathophys Exam 2 Flashcards
Common causes for iron deficiency anemia
{low iron due to blood loss or poor intake}
deficient nutritional intake, gastrointestinal bleeding, hemorrhoids, pregnancy, excessive aspirin intake
common clinical manifestations of anemia
cardio- chest pain (angina), tachycardia, palpitations
respiratory - dyspnea, SOB, increase in RR
neuro - fatigue, headache, faintness
musco- weakness, exercise intolerance
GI - jaundice
GU- decreased urine output
integumentary - pallor
what is innate immunity? 3 main things
the body’s first and immediate line of defense; includes macrophages, cytokines, and natural killer cells.
what is the connection between epithelial cells and innate immunity?
epithelial cells block stuff from coming in, for example the skin, nasal epithelium, mucus, hairs lining tracts, tears, urine, sweat
what is the relationship between natural killer cells and innate immunity?
natural killer cells amplify inflammatory response and kill foreign agents
what is the connection between dendritic cells and innate immunity?
they function as antigen presenting cells to initiate adaptive immunity
what is adaptive immunity? What does it include?
includes cell mediated (aka T-lymphocyte) and humoral (B lymphocyte) immunity. it is slower but capable of targeting specific microorganisms. it includes both active acquired and passive acquired
what are 2 links between innate and adaptive immunity?
1) dendritic cells are essential component of both and link them by releasing cytokines and chemokines
2) cytokines are an essential component of host defense mechanisms and primary means of communicating
what are chemokines?
a subset of cytokines, small protein that act as chemoattractants involved in immune and inflammatory responses
what are 4 major cytokines?
1) interleukins (ILs)
2) Interferons (IFNs)
3) Tumor necrosis factor alpha (TNF-a)
4) chemokines
how is active acquired immunity obtained?
through exposure to an antigen or through immunization or through having the disease. the patient’s body has to synthesize specific immunoglobulins against the antigen. antibodies are formed. long term!
how is passive acquired immunity obtained?
the body passively accepts the immunoglobulins and does not have to manufacture them. it is shorter term. examples are pregnancy (mother-fetus), through the breast milk (mother-baby)
what is the difference between an antibody and an antigen?
an antigen is the substance that induces the formation of an antibody because the immune system recognizes the antigen as a threat
are immunoglobulins and antibodies the same?
yes!
how does humoral immunity work?
uses antibodies to tag pathogens for destruction, think B-lymphocytes – BaHAHA - humoral, antiBodies
IgG
most abundant
the only immunoglobulin that is transported across the placenta
responds to viruses and bacteria
IgM
first antibody to appear in response to antigen
first antibody made by newborn (doesn’t cross the placenta tho)
IgE
mediator of allergic responses
stimulates the release of mast cell - histamine
IgA
seen on body surfaces
in saliva, sweat, tears, mucus, biles, colostrum
why do we care about different immunoglobulins?
increases in specific immunoglobulins help us figure out what is happening
what is the purpose of inflammation?
to eliminate cause of cell injury, remove damages tissue, and generate new tissue
what different cells are associated with the two types of inflammation?
neutrophils with acute (which lasts minutes to several days)
lymphocytes, macrophages and fibrosis tissue are associated with chronic inflammation (days to years)
what is the systemic response to inflammation?
elevated temp=cytokines and prostaglandins
elevated C-reactive protein (CRP) =cytokines
elevated erythrocyte sedimentation rate (ESR) =cytokines
elevated white blood cells=neutrophil production increased by interleukins
malaise and anorexia=cytokines
lymphadenitis= inflammation
what are the two phases of acute inflammation?
1) vascular phase –> increase in blood flow and changes to blood vessels minimize the damage
2) cellular phase –> migration of WBCs for tissue repair, then leukocyte to neutrophil activation and phagocytosis
vascular stage of acute inflammation in detail
immediate vasoconstriction to stop bleeding, followed by vasodilation
this causes the release of histamine and nitric oxide
a protein rich fluid called exudate leaves the vasculature and enters the extravascular space leading to edema, swelling, pain, and impaired function
the loss of fluid allows for clot formation
also increased capillary permeability
what is the end goal of the cellular stage of acute inflammation?
the movement of WBCs to the are of injury and the release of chemical mediators from tissue cells (mast cells and macrophages)
what cells are the first to respond? How long do they last
neutrophils! they have a short life span of 10 hrs
they release hydrogen peroxide and nitric oxide to destroy debris
what is a left shift?
when more immature neutrophils (called bands) are in circulation because of increased demand. this suggests the body is fighting
this might be seen if an infection is occurring that is using up all the mature neutrophils
mature neutrophils are called “segs”
where do macrophages come in? what do they do?
they go in after neutrophils to phagocytize, a similar process to neutrophils
the release prostaglandins, leukotrienes, platelet activating factor, inflammatory cytokines and growth factors
last longer than neutrophils
what does the inflammatory mediator histamine 1 cause?
-vasodilation
-vascular permeability
-bronchoconstriction
what does the inflammatory mediator prostaglandins cause?
vasodilation
vascular permeability
fever
pain
neutrophil chemotaxis – the attractive forces that pull phagocytes to the site of injury
what does the release of inflammatory mediator leukotrienes lead to?
vascular permeability
smooth muscle contraction, which promotes bronchoconstriction and airway edema
slower and more prolonged responses than histamine
what is an ulceration
a site of inflammation that has become necrotic or eroded
what is a type 1 hypersensitivity reaction?
immediate severe allergic response
IgE binds to mast cells and combines with an antigen is previously exposed
-involves CD4 cells, IgE antibodies, eosinophils, and mast cells
key point is too much IgE response
what is a type 4 hypersensitivity reaction?
T-lymphocytes with previous exposure to antigen attacks days later delayed, usually more skin rxn. like poison ivy
which hypersensitivity is related to an antibody-mediated disorder?
type 2 – Transfusion! cytotoxic
what would an elevated eosinophil level means?
an allergic reaction or a parasitic infection
what are two things that the chemical mediators prostaglandins and histamine lead to?
pain and vasodilation
what is an abscess
a localized area of inflammation that contains a purulent exudate, possibly surrounded by a neutrophil layer
Interleukins
Produced by macrophages, generate suppression or enhancement of inflammatory process
Interfeurons
Produced by macrophages, they protect the host agains viral infections and modulate inflammatory response
Tumor necrosis factor alpha
Produces a fever, induces synthesis of pro inflammatory substances in the liver
Prolonged exposure leads to clot formation!
4 types of exudate
1) serous: watery fluid that is amber or clear
2) hemorrahagic: contains RBCs is red/pink
3) fibrinous: thick sticky mesh
4) purulent: pus, degraded WBCs and tissue debris, yellow/white/green
How does cell mediated immunity work?
Think helper T cells!
1)Phagocyte eats bacteria
2)part of the bacteria/antigen goes to the surface of the phagocyte
3)phagocyte presents the antigen to a helper T cell
4) helper T cell is now activated! 🤠
what is a type three hypersensitivity reaction?
lupus, serum sickness, SLE
it is immune complex mediated
T lymphocyte
Continue to mature in the thymus gland where they become
CD4 and CD8 cells and then move to the lymphoid tissue for
proliferation
what is blood composed of?
plasma, RBCs, WBCs, thrombocytes (plateletes)
hematopoiesis
the process of blood cell production:
all cells originate from the pluripotent stem cells in bone marrow
then they divide into myeloid cells and lymphatic cells
blast cells
immature, precursor cells that will mature into the final cells
RBCs, Thrombocytes, basophils, eosinophils, neutrophils, monocytes, B lymphocytes, and T lymphocytes
where do B lymphocytes mature? Where do T lymphocytes mature?
b- bone marrow, T- thymus
what are the 3 key components for RBC synthesis? What organ stimulates the growth of RBCs?
folic acid, vitamin B12, and iron are needed. the kidney releases erythropoietin to stimulate the growth of RBCs with decreased oxygenation
RBC destruction
RBC’s enter the spleen and hemoglobin is removed. The iron in the heme is released by the spleen and returns to the bone marrow for new RBCs. The other part of heme is bilirubin, and is removed from the blood by the liver. the globin is reused as an amino acid.
what happens with unconjugated bilirubin when RBC destruction increases?
it increases, and leads to jaundice
how could someone be hypoxic or have hypoxemia but not be anemic?
if they are drowning, they can’t get any new air into their lungs so they are hypoxic and there might be hypoxemia in the blood. But there is nothing wrong with the number of circulating RBCs or hemoglobin
“emia”
blood issue – example Hypoxemia means decreased oxygenation in the blood
four primary causes of anemia
1) excessive loss of RBCs
2) destruction of RBCs
3) defective RBC production
4) inadequate RBC production due to bone marrow
normocytic-normochromic anemia
rapid hemorrhage or bleeding
clinical manifestations: hypotension, tachycardia, tachypnea, oliguria (low urine output)
microcytic hypochromic anemia
iron-deficiency anemia, cells are pale and small
patho: not being able to synthesize hemoglobin
diagnostic: low MCV, low MCHC
what are the commonalities between vitamin B12 and folic acid deficiency?
both are macrocytic anemia. like prepubescent. B12 and folic acid help RBCs slim down to their sexy mature selves
increased MCV (large RBC size)
vitamin B12 deficiency
B12 is a cofactor for both
#1 synthesis of DNA in RBCs
#2 myelin synthesis of neurons
without B12, folic acid cannot be activated to participate in DNA synthesis
clinical manifestations are the same as anemia but there is also neuro damage due to the demyelination of the central nervous system
pernicious anemia
a specific type of vit B12 anemia.. not being able to absorb it because the body is not producing intrinsic factor
folic acid deficiency
most common in pregnant and lactating women, alcohol abuser
does not show symptoms of anemia until the hematocrit drops below 20%
why is it important to decipher folic acid deficiency from vitamin B12 deficency?
assuming it is folic acid deficiency and administering folic acid can mask a B12 deficiency and neuro dysfunction can still occur
aplastic anemia
disruption of bone marrow function inhibits manufacturing of all blood cells
generally occurs due to toxic substances or infections
hemolytic anemia
caused by rupture of RBCs (hemo-lysis)
acquired: during drug reactions, transfusion reactions, blood type incompatibility with mother-fetus
inherited: sickle cell, thalassemia
diagnose: bone marrow is hyper active, resulting in circulating reticulocytes (immature RBCs)
what does RH- mean
they dont express the D antigen and WILL make RH antibodies . (you cant give RH+ blood to someone that is RH-)
if a person is Type A+, who can they give blood to? who can they receive blood from?
give blood to A+, AB+
can receive blood from A+, A-, O+, O-
what blood type is the universal donor? What blood type is the universal receiver?
O- is the universal donor, AB+ is the universal receiver
if someone is B-, who can they give blood to and who can they receive blood from?
can give blood to B+, B-. AB+, AB-
hemolytic transfusion reaction
recipient blood attacks a donors blood
happens rapidly!
clinical manifestation: fever chills, dypsnea, anaphylaxis
non-hemolytic blood transfusion reaction
delayed (1-6hrs)
people develop antibodies from prior transfusions
sickle cell disease
inherited recessive disorder
abnormal hemoglobin
worry about infections and organ failure
Thalassemia
genetic disorder that affects hemoglobin synthesis
polycythemia
the opposite of anemia
overabundance of RBCs
hemotocrit greater than 47%
primary: hyperproliferation of all cells
secondary: hyperproliferation of RBCs in response to chronic blood hypoxia (COPD)
leukopenia, what is the normal absolute neutrophil count (ANC)?
decreased number of leukocytes in the blood (in many cases that is neutrophils)
ANC greater than 1500 is normal
hematologic neoplasms/cancer
cancer that affects blood, bone marrow and lymph nodes
-located in blood – leukemia
-located in lymph nodes – lymphoma solid mass
why would bone pain be a clinical manifestation of hematologic cancers?
the bone marrow is working so hard to produce more RBCs and is being overcrowed and stretched due to growth
physical assessment diagnostics of hematological cancers
enlarged lymph nodes, splenomegaly (enlarged spleen)
high WBCs
ALL vs AML
acute lymphocytic leukemia (ALL) affects children, acute myelogenous leukemia (AML) affects adults
both present with an abrupt onset of symptoms, need a bone marrow biopsy
Chronic Lymphocytic Leukemia (CLL) vs Chronic Myelogenous Leukemia (CML)
CLL– often incidental finding (WBC is greater than 120,000) b/c of exposure to herbicides
CLM – most have philadelphia chromosome
Multiple Myeloma
happens when people are older
proliferation of abnormal plasma cells
CRABI -
hyperCalcemia
Renal failure
Anemia (decreased production of RBC)
Bone pain
Infection
hodgkins lymphoma
abnormal cells – reed sternberg cells that look like owls eyes
intermittent fever without signs of infection
fatigue
weight loss
multiple node involvement
non-hodgkins lymphoma
chromosomal translocations
accounts for most of lymphoma cases, more likely in older and male adults
derived from either abnormal B or T cells
B symptoms
fever, night sweats, weight loss. if no B symptoms, then considered A=no symptoms
causes of bleeding disorders
factor depletion
lowered production
lowered platelets
more consumption
liver dysfunction
vitamin k deficiencies
hemostasis
clotting process
1) vascular spasm
2) platelet plug formation
3) coagulation
4) clot retraction
5) clot lysis
clinical manifestations of a bleeding disorder
nose bleed, purpura, bleding gums, abnormal vaginal bleeding, decreased platelets (less than 20,000 can cause spontaneous bleeding), enlarged spleen
ITP (immune thrombocytopenia purpura)
autoimmune disorder, follows viral diseases
antibodies will destroy platelets
TTP (thrombotic thrombocytopenia purpura)
inherited or acquired
different from ITP because in TTP, the platelets will start to adhere together forming clots that can clog the vascular system. similar to HIT
heparin induced thrombocytopenia (HIT)
when given the anticoagulant drug heparin,
immune response where platelets are activated and start making clots
also clot formations forming (like TTP)
DIC
overreaction of an inflammatory response
can be mild or cause death
hemophilia A/B
inherited disorders that primarily affect males (X linked recessive)
causes bleeding anywhere
A is caused by lack of factor 8 (more common)
B is caused by lack of factor 9
