Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

UCAN > Pathophys Exam 2 > Flashcards

Pathophys Exam 2 Flashcards

1
Q

Common causes for iron deficiency anemia

A

{low iron due to blood loss or poor intake}
deficient nutritional intake, gastrointestinal bleeding, hemorrhoids, pregnancy, excessive aspirin intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

common clinical manifestations of anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is innate immunity? 3 main things

A

the body’s first and immediate line of defense; includes macrophages, cytokines, and natural killer cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the connection between epithelial cells and innate immunity?

A

epithelial cells block stuff from coming in, for example the skin, nasal epithelium, mucus, hairs lining tracts, tears, urine, sweat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the relationship between natural killer cells and innate immunity?

A

natural killer cells amplify inflammatory response and kill foreign agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the connection between dendritic cells and innate immunity?

A

they function as antigen presenting cells to initiate adaptive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is adaptive immunity? What does it include?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are 2 links between innate and adaptive immunity?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are chemokines?

A

a subset of cytokines, small protein that act as chemoattractants involved in immune and inflammatory responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are 4 major cytokines?

A

1) interleukins (ILs)
2) Interferons (IFNs)
3) Tumor necrosis factor alpha (TNF-a)
4) chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is active acquired immunity obtained?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is passive acquired immunity obtained?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the difference between an antibody and an antigen?

A

an antigen is the substance that induces the formation of an antibody because the immune system recognizes the antigen as a threat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

are immunoglobulins and antibodies the same?

A

yes!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does humoral immunity work?

A

uses antibodies to tag pathogens for destruction, think B-lymphocytes – BaHAHA - humoral, antiBodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IgG

A

most abundant
the only immunoglobulin that is transported across the placenta
responds to viruses and bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IgM

A

first antibody to appear in response to antigen
first antibody made by newborn (doesn’t cross the placenta tho)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

IgE

A

mediator of allergic responses
stimulates the release of mast cell - histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

IgA

A

seen on body surfaces
in saliva, sweat, tears, mucus, biles, colostrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

why do we care about different immunoglobulins?

A

increases in specific immunoglobulins help us figure out what is happening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the purpose of inflammation?

A

to eliminate cause of cell injury, remove damages tissue, and generate new tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what different cells are associated with the two types of inflammation?

A

neutrophils with acute (which lasts minutes to several days)
lymphocytes, macrophages and fibrosis tissue are associated with chronic inflammation (days to years)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the systemic response to inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the two phases of acute inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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
26
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)
27
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
28
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"
29
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
30
what does the inflammatory mediator histamine 1 cause?
-vasodilation -vascular permeability -bronchoconstriction
31
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
32
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
33
what is an ulceration
a site of inflammation that has become necrotic or eroded
34
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
35
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
36
which hypersensitivity is related to an antibody-mediated disorder?
type 2 -- Transfusion! cytotoxic
37
what would an elevated eosinophil level means?
an allergic reaction or a parasitic infection
38
what are two things that the chemical mediators prostaglandins and histamine lead to?
pain and vasodilation
39
what is an abscess
a localized area of inflammation that contains a purulent exudate, possibly surrounded by a neutrophil layer
40
Interleukins
Produced by macrophages, generate suppression or enhancement of inflammatory process
41
Interfeurons
Produced by macrophages, they protect the host agains viral infections and modulate inflammatory response
42
Tumor necrosis factor alpha
Produces a fever, induces synthesis of pro inflammatory substances in the liver Prolonged exposure leads to clot formation!
43
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
44
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! 🤠
45
what is a type three hypersensitivity reaction?
lupus, serum sickness, SLE it is immune complex mediated
46
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
47
what is blood composed of?
plasma, RBCs, WBCs, thrombocytes (plateletes)
48
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
49
blast cells
immature, precursor cells that will mature into the final cells RBCs, Thrombocytes, basophils, eosinophils, neutrophils, monocytes, B lymphocytes, and T lymphocytes
50
where do B lymphocytes mature? Where do T lymphocytes mature?
b- bone marrow, T- thymus
51
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
52
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.
53
what happens with unconjugated bilirubin when RBC destruction increases?
it increases, and leads to jaundice
54
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
55
"emia"
blood issue -- example Hypoxemia means decreased oxygenation in the blood
56
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
57
normocytic-normochromic anemia
rapid hemorrhage or bleeding clinical manifestations: hypotension, tachycardia, tachypnea, oliguria (low urine output)
58
microcytic hypochromic anemia
iron-deficiency anemia, cells are pale and small patho: not being able to synthesize hemoglobin diagnostic: low MCV, low MCHC
59
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)
60
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
61
pernicious anemia
a specific type of vit B12 anemia.. not being able to absorb it because the body is not producing intrinsic factor
62
folic acid deficiency
most common in pregnant and lactating women, alcohol abuser does not show symptoms of anemia until the hematocrit drops below 20%
63
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
64
aplastic anemia
disruption of bone marrow function inhibits manufacturing of all blood cells generally occurs due to toxic substances or infections
65
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)
66
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-)
67
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-
68
what blood type is the universal donor? What blood type is the universal receiver?
O- is the universal donor, AB+ is the universal receiver
69
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-
70
hemolytic transfusion reaction
recipient blood attacks a donors blood happens rapidly! clinical manifestation: fever chills, dypsnea, anaphylaxis
71
non-hemolytic blood transfusion reaction
delayed (1-6hrs) people develop antibodies from prior transfusions
72
sickle cell disease
inherited recessive disorder abnormal hemoglobin worry about infections and organ failure
73
Thalassemia
genetic disorder that affects hemoglobin synthesis
74
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)
75
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*
76
hematologic neoplasms/cancer
cancer that affects blood, bone marrow and lymph nodes -located in blood -- leukemia -located in lymph nodes -- lymphoma *solid mass*
77
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
78
physical assessment diagnostics of hematological cancers
enlarged lymph nodes, splenomegaly (enlarged spleen) high WBCs
79
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
80
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
81
Multiple Myeloma
happens when people are older proliferation of abnormal plasma cells CRABI - hyperCalcemia Renal failure Anemia (decreased production of RBC) Bone pain Infection
82
hodgkins lymphoma
abnormal cells -- reed sternberg cells that look like owls eyes intermittent fever without signs of infection fatigue weight loss multiple node involvement
83
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
84
B symptoms
*fever, night sweats, weight loss*. if no B symptoms, then considered A=no symptoms
85
causes of bleeding disorders
factor depletion lowered production lowered platelets more consumption liver dysfunction vitamin k deficiencies
86
hemostasis
clotting process 1) vascular spasm 2) platelet plug formation 3) coagulation 4) clot retraction 5) clot lysis
87
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
88
ITP (immune thrombocytopenia purpura)
autoimmune disorder, follows viral diseases antibodies will destroy platelets
89
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
90
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)
91
DIC
overreaction of an inflammatory response can be mild or cause death
92
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

UCAN (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions