Final Exam 1 Flashcards
Genetics, Altered Cells, Immunology, Cancer, Fluids/Acid-Base, Neuro, Renal
<p>silent, missence, and nonsense are all what type of genetic mutation</p>
<p>base pair substitution</p>
<p>mutation -> new codon -> same AA</p>
<p>silent mutation</p>
<p>mutation -> new codon -> new AA</p>
<p>missense mutation</p>
<p>mutation -> new codon -> stop codon</p>
<p>nonsense mutation</p>
<p>insertion or deletion of 1 or more base pairs</p>
<p>frameshift mutation</p>
<p>Chromosomes and pairs of somatic cells</p>
<p>46 chromosomes in 23 pairs (diploid)</p>
<p>Chromosomes and pairs of gametes</p>
<p>23 chromosomes as singles (haploid)</p>
<p>cells w/ a multiple of the normal number of chromosomes</p>
<p>euploid cells</p>
<p>cells w/ compete extra sets of chromosomes</p>
<p>polyploidy (usually spontaneous aborted or stillborn)</p>
<p>describe the chromosomes in triploidy and tetraploidy cells</p>
<p>- triploidy = 3 complete sets of chromosomes- tetraploidy = 4 complete sets of chromosomes</p>
<p>a cell that does not contain a multiple of 23 chromosomes (missing or additional individual chromosomes)</p>
<p>aneuploidy</p>
<p>name 2 types of aneuploidy cells and which type is worse</p>
<p>monosomy and trisomy; monosomy is worse due to the lack of genetic material</p>
<p>aneuploidy is a result of what?</p>
<p>nondisjunction - homologous chromosomes or sister chromatids fail to separate during mitosis or meiosis</p>
<p>intellectual disability, distinctive facial features, and increased risk of leukemia</p>
<p>Down Syndrome/Trisomy 21</p>
<p>short stature, neck webbing, spaced nipples, usually sterile, but no intellectual disability</p>
<p>Turner Syndrome/Monosomy X</p>
<p>breast development, small testicles, typically sterile and some intellectual impairment</p>
<p>Klinefelter Syndrome/XXY condition</p>
<p>low birth weight, severe intellectual disability, microcephaly, heart defects, and characteristic high pitched cry</p>
<p>Chromosome 5 - deletion of short arm/Cri-du-chat syndrome</p>
<p>Name 4 types of abnormalities in chromosome structure</p>
<p>- deletion- duplication- inversion- translocation</p>
<p>exchange of material between 2 non-homologous chromosomes</p>
<p>reciprocal translocation</p>
<p>long arms of 2 non-homologous chromosomes combine at the centromere to form a single chromosome and the short arms are usually lost</p>
<p>Robertsonian translocation</p>
<p>On what chromosomes do Robersonian translocations occur?</p>
<p>13, 14, 15, 21, and 22</p>
<p>more common in males; causes intellectual disability (2nd most common under Down syndrome)</p>
<p>gap on long arm of X chromosome/Fragile X Syndrome</p>
<p>Patau syndrome</p>
<p>trisomy 13</p>
<p>Edward's syndrome</p>
<p>trisomy 18</p>
what is the recurrence of autosomal dominant
50%
List 3 examples of autosomal dominant disorders
Huntington's disease, Von Willebrand's disease, and Marfan's syndrome
% of individuals w/ a genotype who also exhibit the expected phenotype
penetrance
individuals w/ disease-causing genotype but not the phenotype
incomplete penetrance
What is a common example of incomplete penetrance
retinoblastoma - about 90% who carry the gene will get the disease (90% penetrance)
What AD disease is known for its delayed age of onset (about 40 y/o)?
Huntington's disease
What is the recurrence of autosomal recessive?
50% carrier, 25% normal; 25% affected
List 3 examples of AR diseases
cystic fibrosis, sickle cell anemia, and albinism
List 3 examples of X-linked inheritance
color blindness, Duchenne muscular dystrophy, and hemophilia A
range of phenotypes that vary between patients and specific genotype
expressivity
Example of expressivity
neurofibromatosis
traits in which variations are caused by combined effect of multiple genes (polygenic)
multifactorial inhertence
certain number of factors/genes must be affected before phenotype is expressed
threshold of liability
What chromosome is cystic fibrosis linked to?
chromosome 7
Decrease or shrinkage of cell size
atrophy
Increase in size of cells
hypertrophy
Increase in the number of cells (from an increased rate of cellular division)
hyperplasia
Abnormal changes in size, shape, or organization of mature cells
dysplasia
Reversible replacement of one mature cell type by another
metaplasia
What 2 types of cellular adaptation occur in non dividing cells?
atrophy and hypertrophy
Physiologic vs Pathologic atrophy
- Physiologic: normal process that usually occurs in early development (ex. thymus in children)- Pathologic: due to decreased pressure, use, blood, nutrition, hormones, or stimulation (ex. disuse atrophy in skeletal muscle)
chronic malnutrition atrophy is often accompanied by what?
autophagy -> autophagic vacuoles contain cellular debris and enzymes
Physiologic vs Pathologic cardiac hypertrophy
Physiologic: temporary and preserves myocardial structure (ex. endurance training, postnatal development, and pregnancy)Pathologic: includes aging, strenuous exercise, sustained workload or stress
Explain compensatory hyperplasia. Where is it significant?
adaptive and allows for some organs to regenerate(epidermal and intestinal epithelia, hepatocytes, BM cells, and fibroblasts)
Explain hormonal hyperplasia
occurs in estrogen-dependent organs in response to hormonal stimulation (uterus and breast)
Explain pathologic hyperplasia
abnormal proliferation of normal cells (usually in response to excessive hormonal stimulation or GF on those cells)
2 most common examples of pathologic hyperplasia
- hyperplasia of the endometrium (over secretion of estrogen)- BPH (due to changes in hormonal balance)
Dysplasia is also known as what?
atypical hyperplasia -> not a true adaptive change
T/F: Dysplasia means the presence of cancer
False; dysplasia does NOT indicate cancer and may not progress to cancer if stimulus is removed early on
If metaplasia is not reversed, what can it advance to?
Dysplasia and possible cancerous transformations
Explain the general mechanisms of cellular injury (regardless of cause)
- depletion of ATP - mitochondrial damage - O2 and O2-derived free radical membrane damage - protein folding defects - DNA damage - calcium level changes
Most common cause of hypoxia
ischemia (reduced blood supply)
What causes ischemia
narrowing of arteries (arteriosclerosis) or complete occlusion by clots (thrombosis)
Explain what causes a cell to swell w/ hypoxic injury
decreased mitochondrial O2 -> decreased ATP -> Na/K pump failure -> increased intracellular Na -> increased intracellular H2O -> swelling
Explain what causes a decrease in protein synthesis w/ cellular hypoxic injury
increase intracellular H20 -> dilation of ER -> detachment of ribosomes
Explain what causes nuclear chromatin clumping w/ cellular hypoxic injury
decrease in O2 -> decrease in ATP -> increase anaerobic glycolysis -> decrease glycogen -> increase lactate -> decrease pH -> chromatin clumping & DNA damage
Explain changes to Na, K, and Ca during cellular hypoxic injury
- increased intracellular Na- increased extracellular K- increased intracellular Ca
Where is intracellular Ca released from?
mitochondria and smooth ER
Name 4 mechanisms for ischemia-reperfusion injury
- oxidative stress- increased intracellular Ca- inflammation- complement activation
Name 3 types of reactive oxygen species (ROS)
- hydroxyl radical (OH-)- superoxide radical (O-)- hydrogen peroxide (H2O2)
How does cell structure change after reperfusion injury?
ischemic cell = swollen | reperfusion injured cell = necrotic
main systems affected by lead (Pb)
nervous system and blood
carbon tetrachloride (CCl4) affects what organ
liver
Explain how CO causes hypoxic injury
has a higher affinity for hemoglobin than O2 -> carboxyhemoglobin
Sxs of CO poisoning
dizziness, weakness, N/V, headache, tinnitus, confusion, and chest pain
Primary systems affected by ethanol
brain and liver
What nutrition deficiencies are associated w/ ethanol?
Mg, B6, thiamine, and phosphorus; folic acid is a problem for chronic drinkers
bleeding into skin or underlying tissues -> takes time to appear
contusion (bruise)
collection of blood in soft tissue that appears quickly
hematoma
wound is longer than it is deep -> usually has significant external bleeding w/ little internal bleeding
incised wound
penetrating sharp-force injury deeper than it is long
stab wound
produced by items w/ sharp points but dull edges (ex. stepping on a nail)
puncture wound
What will affect the appearance of an entrance gunshot wound?
range of the gunshot
What is seen w/ contact range entrance gunshot wound?
- searing of the edges- blowback (gaping or jagged)- muzzle imprints
What is seen w/ intermediate range entrance gunshot wound?
- tattooing/stippling: fragments of gunpowder abrade but don't enter the skin
appearance is the same regardless of range
indeterminate range entrance wound AND exit wound
Necrosis vs Apoptosis
- Necrosis: unprogrammed death; cellular swelling -> lysis; inflammation; many cells affected - Apoptosis: programmed, organized disassembly; membrane bound shrinkage; no inflammation; one cell or small clusters
nucleus gets smaller -> DNA condenses into shrunken particles
pyknosis
fading away of nuclear envelope and nuclear material
karyolysis
nuclear fragmentation
karyorrhexis
Explain coagulative necrosis and where it occurs
- ischemia -> decrease pH -> protein degeneration -> albumin becomes firm and opaque
- occurs in kidneys, heart, adrenal glands
Explain liquefaction necrosis and where it occurs
- autolysis (hydrolytic enzymes) and heterolysis (bacterial infection) -> tissue becomes soft, liquefies, and segregates -> forms cysts
- occurs in neurons and glial cells of the brain
Types of bacteria involved in liquefaction necrosis?
- Staph- Strep- E. Coli
Explain caseous necrosis
- mycobacterium (TB) is walled off in a granuloma -> cells disintegrate but not completely digested (combo of coagulative and liquefaction) - will resemble cottage cheese (soft and granular)
Explain fat necrosis and where it occurs
- occurs by lipases -> break down triglycerides -> release FAs that combine w/ Ca, Mg, and Na (saponification) -> white and chalky
- occurs in the breast, pancreas, and other ABD organs
Dry vs wet gangrene
- Dry: poor perfusion (coagulative necrosis)- Wet: poor perfusion + pyogenic infection (liquefactive necrosis)
Explain gas gangrene
caused by species of Clostridium -> produces hydrolytic enzymes and toxins -> destroy connective tissue and membranes -> gas bubble form in muscle cells -> death caused by shock
What occurs during algor mortis?
- body temp decreases 1 degree per hour- by 24 hours -> body temp = environment
What is the main event of livor mortis and how it is physically seen?
- blood pools at the lowest point of the body (due to gravity)- purple discoloration where blood pools (line of demarcation)- can see pupils dilate and become nonreactive to light due to decreased retinal pressure (decrease muscle tension)
What is the timeframe for rigor mortis? What causes rigor mortis?
- starts within 6 hours after death and lasts for approximately 36 hours (then body becomes flaccid)
- acid builds up in muscles -> delete ATP -> myosin doesn't work for relaxation -> rigid muscles (small muscles first)
What is postmortem autolysis (putrefaction)?
breakdown of tissues that occurs between 24-48 hours (all cells start necrosing)
What speeds up/slows down the process of postmortem autolysis?
- warm environment speeds it up- cold slows it down
Lines of defense (3)
- 1st: innate (natura/native) immunity- 2nd: inflammation- 3rd: adaptive (acquired) immunity
What 3 things are part of innate immunity?
- physical barriers- epithelial cell-derived chemicals- normal microbiome
List 4 characteristics of the inflammatory response
- occurs in vascularized tissues- activates rapidly (in seconds) after damage occurs- depends on activity of both cellular and chemical components- nonspecific
At the beginning of the inflammatory reaction, what are 3 vascular responses that occur?
- vasodilation- increased vascular permeability- WBC adherence to the inner walls of vessels and migration through vessels
What causes edema at the site of injury?
increased vascular permeability -> plasma proteins leak from capillary bed -> oncotic pressure -> fluid will follow protein out of capillary -> edema
Who are the 1st and 2nd responders at a site of inflammation?
1st responder: neutrophil2nd responder: macrophage (from monocyte)
List the 3 plasma systems
- complement- clotting- kinin
Symptoms of acute inflammatory response and causes?
- vasodilation (erythema/warmth)- vascular permeability (edema)- cellular infiltration (pus)- thrombosis (clots) -> helps encapsulate bacteria- stimulation of nerve endings by kinin (pain)
cells filled w/ granules and located in loose connective tissue close to blood vessels
mast cells
What 3 types of granules are released by mast cells?
- histamine- chemotactic factor for neutrophils- chemotactic factor for eosinophils
List 3 mediators synthesized by mast cells
- platelet activating factor (PAF)- prostaglandins- leukotrienes
Function of PAF
platelet activation and vasodilation
Function of prostaglandins
increased vascular permeability, neutrophil chemotaxis, and pain
Explain histamine's function after being released from mast cells
vasoactive: temporary rapid constriction of large blood vessels and dilation of post-capillary venues; retraction of endothelial cells lining capillaries (junctions)
Explain the compliment system
- C3 -> C3b + C3a- C3b -> C5 -> C5b + C5a- C5b -> C6-9 -> membrane attack complex- MAC forms pores in pathogen membrane to damage it
What in the compliment system creates opsonin? What is the function of opsonin?
- C3b- coats surface of bacteria and increases their susceptibility to phagocytosis
potent anaphylatoxin in the compliment system -> mass cell release of histamine
C3a
Anaphylatoxin and chemotactic factor in compliment system -> leukocyte (neutrophil) migration
C5a
main protein in a blood clot
fibrin
What activates the extrinsic pathway of the clotting system?
tissue factor (TF) - released by damaged endothelial cells in blood vessels (external trauma)
What activates the internal pathway of the clotting system?
activated when the vessel wall is damaged (trauma inside the blood vessels)
- Factor unique to extrinsic pathway- Factor unique to intrinsic pathway- Factor activated by both pathways
- Extrinsic: VIIa- Intrinsic: XII (Hageman Factor) -> XIIa- Both: Xa
Describe the common pathway of the clotting cascade
Xa -> thrombin -> fibrinogen -> fibrin -> blood clot
functions to activate and assist inflammatory cells; interacts closely w/ coagulation system
Kinin system
What activates the kinin system?
activation of Hageman factor (XII) to XIIa (aka prekallikrein)
Functions of bradykinin
- vasodilation (like histamine)- induce pain (w/ prostaglandins)- smooth muscle contraction- increase vascular permeability- leukocyte chemotaxis
Cytokines that cause vasodilation (3)
- prostaglandins- histamine- NO
Cytokines that cause vascular permeability (4)
- histamine- bradykinin- leukotrienes- PAF
Cytokines that cause pain (2)
- prostaglandins- bradykinin
Cytokines that cause fever (4)
- IL-1- IL-6- TNF-a- prostaglandins
Cytokines that activate leukocytes (2)
- IL-1- TNF-a
activate T-cells without MHC-II or antigen to activate them -> widespread activation of immune system
Superantigens
List acute phase reactants (5)
IL-1, IL-6, IL-8, TNF-a, and C-reactive protein
What does C-reactive protein tell about inflammation
global test for inflammation (doesn't tell cause or location; only that it exists)
increased neutrophils?
acute bacteria/acute inflammation
increased lymphocytes?
viral infection/chronic bacterial infection
increased monocytes?
inflammation
increased basophils?
allergic reaction
increased eosinophils?
parasitic infection
type of innate lymphocyte
natural killer cell (NK cell)
How do cytokines limit inflammation?
- inhibit production- inhibit macrophage proliferation- destroy histamine and leukotrienes
How do cytokines help w/ repair and healing?
- activate macrophages- stimulate fibroblast growth- stimulate endothelial growth
Explain VEGF function and how it relates to cancer and chemo
- VEGF is angiogenic -> vascular growth- found in some cancers to help them develop blood supply- some chemo targets this -> will also delay healing
What does the erythrocyte sedimentation rate test?
how fast RBCs settle at the bottom of the test tube -> faster may mean inflammation
How do cytokines help w/ phagocytosis?
- adherence and diapedesis- chemotaxis- opsonins- activate and increase macrophages
Type I interferons (IFN)
INF-a and INF-b
Type II interferon (IFN)
IFN-y
IL that is pro inflammatory an endogenous pyrogen (causes fever)
IL-1
IL that directly induces hepatocytes to produce proteins needed for inflammation and stimulate differentiation and growth of BM cells
IL-6
List 3 systemic effects of TNF-a
- induces fever (endogenous pyrogen)- increased synthesis of inflammation proteins by liver- muscle wasting (cachexia) and intravascular thrombosis in cases of severe infection/cancer
What IL is anti-inflammatory?
IL-10
What cells secrete TNF-a?
macrophages
macrophages that predominate in early inflammation and become a component of purulent exudate
neutrophils (PMNs)
Life cycle of monocytes
produced in the BM -> travel to site of inflammation about 24 hours after neutrophils -> develop into macrophages
defense against parasites and regulation of vascular mediators
eosinophils
adherence of leukocytes to endothelial cells
margination
emigration of cells through endothelial junctions
diapedesis
protein filled watery exudate that indicates early inflammation
serous
thick, clotted exudate -> indicates more advanced inflammation
fibrinous
pus filled exudate that indicates bacterial infection or inflammation (supperative)
purulent
2 types of exudate that indicate bleeding
serosanguinous and sanguinous
Risks that lead to dysfunctional wound healing
- hemorrhage- fibrous adhesion- hypovolemia- lack of nutrients- poor control of glucose levels- infection
raised scar from original skin level (4mm above skin)
keloid scar
scar that is larger than it should be
hypertrophic
process by which the extensive diversity of antigen receptors on B and T cells is established
clonal diversity
develop from B cells -> produce antibodies
plasma cells
T cells that identify and kill target cells
cytotoxic T cells
come from both B and T cells and activate rapidly during a second infection w/ the same microbe
memory cells
infection/exposure immunity
active natural
vaccine immunity
active artificial
maternal immunity
passive natural
IVIg (immunoglobulins/serum/antibodies)
passive artificial
T/F: passive immunity does not lead to memory
True
3 parts to an antibody
- 2 identical antigen binding fragments (Fab)- Fc portion that is responsible for most biological functions of antibody
How do Abs indirectly affect Ags
activate innate immune system -> complement and phagocytes
best complement activating antibody
IgM
best opsonin antibody
IgG
antibody that is part of mucosal immunity
IgA
antibody that responds to allergic reactions and parasites to activate mast cells
IgE
only antibody that crosses the placenta
IgG
processing of antigen and gene rearrangement for a specific immune response
clonal selection
Which cells are APCs
dendritic cells, macrophages, and B cells
What cells are HLA class II found on
all APCs
What cells are HLA class I found on
all nucleated cells
What is presented by each class of HLA and to what cells are they presented?
- HLA I: present endogenous antigens for cytotoxic T cells (CD8) -> gives thumbs up that the cell is okay - HLA II: present exogenous antigens ingested to T-helper cells (CD4) -> activate adaptive immunity
T/F: APCs have both HLA I and HLA II on their surface
True: all nucleated cells have HLA I
What immunoglobulins do B cells produce before class switching?
IgM and IgD
immunoglobulins released during primary exposure
IgM (major) and IgG (minor)
immunoglobulins released during secondary exposure
IgG (major) and IgM (minor)
Most abundant immunoglobulin in the body
IgG
ability to produce soluble toxins or endotoxins (greater influence pathogen's degree of virulence)
toxigenicity
opportunistic bacteria that is commonly found on skin and nasal passages but is also a major cause of HAI and abx resistance
staphylococcus aureus
T/F: S. aureus uses biofilms to colonize but doesn't produce toxins
False: produces and secretes exotoxins as well as uses biofilms
proteins created and secreted by the bacteria to have a virulence effect -> can damage plasma membranes or inactivate enzymes needed for protein synthesis
exotoxins
Explain how endotoxins can activate inflammatory response and produce fever
When bacterial cell dies -> membrane is disrupted -> releases LPS (lipid A portion) -> lipid A exposed to the immune system -> causes fever, shock, and DIC
what type of bacteria produce endotoxins?
gram-negative bacteria
Explain what causes endotoxic shock
bacteria growing in blood (septicemia) -> release endotoxins -> activate complement and clotting systems -> increased capillary permeability -> large volumes of plasma escape to surrounding tissues -> hypotension -> shock
antigenic drift vs shift
- antigenic drift: minor change in surface antigens due to mutations -> leads to weakened protection against virus- antigenic shift: major change where genome is segmented and undergoes recombination (usually zoonotic)
What 2 proteins classify influenza and what do they do?
- H protein (hemagglutinin): attachment and fusion (entry into cell)- N protein (neuraminidase): facilitates release of viral proteins from host cell
large microorganisms w/ thick, rigid cell walls without peptidoglycan
fungus/mycoses
- most common cause of fungal infections- opportunistic fungus that is normally found in the skin, GI tract, and vagina but can cause localized infection if overgrown -> disseminates if immunocompromised
Candida albicans
eukaryotic, unicellular microorganisms include malaria, amoeba, and flagellates
protozoa
What causes antibiotic resistance?
- genetic mutations- lack of compliance (selective resurgence)- overuse (destruction of normal microbiome)
Lab/serum tests used to evaluate immunodeficiencies
- CBC w/ diff- quantitative determination of immunoglobulins- assay for total complement
List the 6 stages of viral infection of a host cell
- attachment- penetration- uncoating- replication- assembly- release
What do all viruses contain?
genome and capsid
MOA of most antibiotics (4)
- inhibition of function/production of cell wall/membrane- prevent protein synthesis- blockage of DNA replication- interference w/ folic acid metabolism
x-linked disorder where IgM production is greatly depressed; clinical triad is eczema, thombocytopenia, and immune deficiency
Wiskott-Aldrich Syndrome
What cells are destroyed by HIV? What is the purpose of these cells?
CD4 Th cells -> necessary for development of plasma cells and CD8 cytotoxic T cells
How is HIV spread?
blood-borne and sexual contact (more common)
What do retroviruses use to implant their ds DNA into host cells?
- reverse transcriptase: RNA -> DNA- HIV integrase: inserts DNA into host genes
Describe the general steps of HIV life cycle (6)
- virion binds to CD4 and chemokine receptor- fusion of membrane w/ host cell membrane -> genome enters cytoplasm- reverse transcriptase -> integration of virus genes into host genome- transcription of HIV genome into RNA- synthesis of proteins and assembly of virion core- budding and release of mature vision
current regimen for treatment of HIV (combination of drugs)
antiretroviral therapy (ART)
Name 2 lab tests use to determine the progression of HIV
- HIV RNA levels: determines viral load- CD4 T cell count
Normal CD4 T cell count and value that begins to cause opportunistic infections
- Normal: 800-1000- Opportunistic infections: < 200
Describe typical HIV progression without treatment
- exposure: viral load is high (first 6-12 weeks) - clinical latency: viral load is low (no sxs) but it could still be transmitted (12 weeks - 7 years); CD4 count drops slowly over time - Constitutional sxs as viral load begins increasing - Opportunistic diseases occur as CD4 < 200
Clinical symptoms of AIDS
- cachexia (severe weight loss)- Kaposi sarcoma- PCP pneumonia- other atypical or opportunistic infections or cancers
Hypersensitivity I, II, III are mediated by what? How does this differ from hypersensitivity IV?
- mediated by Abs- Type IV is cell mediated
type I hypersensitivity is mediated by what?
IgE mediated against environmental antigens (allergens)
sensitizing exposure and re-exposure in type I hypersensitivity
- sensitizing exposure: allergen binds to APC -> B cell + Th2 cell -> plasma cell -> creates IgE -> binds to IgE Fc receptor on mast cell- re-exposure: allergen enters -> binds to IgE on mast cells -> mast cell degranulation -> histamine release -> edema/smooth muscle contraction/mucous secretion
Symptoms of type I hypersensitivity
- itching/urticaria- angioedema- hypotension- bronchospasm (anaphylaxis)- dysrhythmia
type II hypersensitivity is mediated by what?
specific cell or tissue (tissue-specific antigens)
Ex. of type II hypersensitivity
- Graves disease (hyperthyroidism)- myasthenia gravis- Hemolytic disease of newborn (HDNB)
type III hypersensitivity is mediated by what?
immune complex mediated (not organ specific) -> antigen-antibody complex circulate and later deposited in vessel walls or extravascular tissues
Ex. of type III hypersensitivity
- serum sickness (includes Raynaud phenomena)- arthus reaction- SLE
type IV hypersensitivity is mediated by what?
cell-mediated; either cytotoxic T lymphocytes or lymphokine-producing Th1 and Th17 cells -> direct killing of target cells
Ex. of type IV hypersensitivity
- graft rejection- TB skin test- contact dermatitis (poison ivy, metals, and latex)
autoimmune disease characterized by production of a large variety of antibodies (autoantibodies)
systemic lupus erythematosus (SLE)
Explain how SLE is a type III hypersensitivity
causes deposition of circulating immune complexes containing antibody against host DNA
List some of the clinical manifestations of SLE
- arthritis/arthralgia - vasculitis/rash - renal disease - hematologic changes - CV disease - photosensitivity - presence of ANA (antinuclear antibodies) in blood
3 types of transplant rejection
- hyperacute: due to preexisting ab to the antigens of the graft - acute: cell-mediated immune response (type IV) against unmatched HLA antigens - chronic: takes months-years; weak cell-mediated reaction against minor HLA antigens
6 characteristics of benign tumors
- grow slowly- well-defined capsule- non invasive (don't grow past capsule)- well differentiated (similar to original cells)- low mitotic index- don't metastasize
6 characteristics of malignant tumors
- grow rapidly- not encapsulated- invasive- poorly differentiated (anaplasia)- high mitotic index- can spread distantly (metastasize)
pre-invasive epithelial malignant tumors of glandular or epithelial origin that have not broken through the basement membrane or invaded surrounding stroma
carcinoma in situ (CIS
What type of benign tumor does cause problems?
brain tumors -> limited space to grow so will affect the functions of surrounding tissues
increase in catecholamines indicates what?
adrenal medullary tumor (ex. pheochromocytoma)
increase in ACTH indicates what?
adrenal, pituitary, or hypothalamic tumors
increase in b-HCG indicates what?
germ cell and hepatic cancers
increase in carcinoembryonic antigen (CEA) indicates what?
colon, lung, pancreas, or breast cancer
alpha fetoprotein (AFP) is used to monitor what types of cancers?
hepatic and germ cell (testicular and ovarian)
CA-125 is used to monitor what type of cancer?
ovarian
What problem has been found with prostate specific antigen (PSA)?
many false positives -> approximately 75% of men w/ increased PSA don't have prostate cancer on biopsy
cancer is mainly a disease of what?
aging
4 types of gene mutations related to cancer
- secretion of growth factors- increased GF receptors- signal on cell-surface receptor is mutated in the "on" position- Intracellular signaling protein to promote replication
genes that regulate normal cellular proliferation
proto-oncogenes
mutation gained in proto-oncogene so that it can't slow down
oncogene
the "guardian of the genome" - signal to undergo apoptosis
p53
How do cancers participate in angiogenesis
secrete angiogenic factors such as vascular endothelial growth factor (VEGF)
Explain how cancer cells use telomeres to become immortal
cancer cells can secrete telomerase to restore and maintain telomeres -> allow for continuous division without stop
List the 6 hallmarks of cancer
- Self-sufficiency (in growth signals)- Evading growth suppressors- Tissue invasion and metastasis- Replication immortality- Induce angiogenesis- Resist cell death (apoptosis
genes tested for breast cancer
BRCA1/BRCA2
hereditary nonpolyposis colorectal cancer (no polyps present -> requires regular screenings)
Lynch syndrome
familial adenomatous polyposis is cancer of the colon/rectum caused by mutations in what gene?
APC
gene associated w/ thyroid cancer
RET
gene associated w/ retinoblastoma
RB1
T/F: most cancer is inherited
False: most is NOT inherited
chronic infections w/ H. pylori are associated w/ what?
- PUD- stomach carcinoma (most stomach cancers)- MALT lymphomas
entry of tumor cells into circulation
intravasation
exit of tumor cells from circulation
extravasion
Most common metastasis sites
brain, bone, liver, and lung
TNM staging
- Tumor: # equals size of tumor and local extent- Node: higher # means more nodes involved- Metastasis: # indicates extent of metastasis
increase in ____ comes from mutations of proto-oncogenes -> oncogenes
pro-growth signals
decrease in ____ comes from mutations in tumor-suppressor genes
anti-growth signals
examples of oncogenes
- c-ras- myc- fos- jun
most common genetic defects found in human cancers
mutations of tumor-suppressor genes
What triggers the extrinsic pathway of apoptosis?
Fas - "death receptor"
What is one of the most important activators of the Fas receptor
TNF-a
T/F: pain is one of the first signs of cancer
False; little/no pain is associated w/ early stage of cancer
What is the most frequently reported symptom of cancer and cancer treatment?
fatigue
What is included in cachexia (5)?
- anorexia- early satiety- weight loss- taste alternation- altered metabolism
Causes of anemia in cancer (4)?
- chronic bleeding due to iron deficiency- severe malnutrition- medical therapies (chemo)- malignancy in blood forming organs
Causes of leukopenia and thrombocytopenia in cancer?
- direct tumor invasion to the bone marrow- chemo drugs are toxic to the bone marrow
symptom complexes triggered by cancer but not caused by direct local effects of the tumor; commonly due to biologic substances released from the tumor or by immune responses triggered by the tumor
paraneoplastic syndrome
in what cancers are paraneoplastic syndromes most often seen?
breast, lung, and ovarian cancer
What system is most affected by paraneoplastic syndromes?
nervous system (can cause various neurological disorders that precede other cancer symptoms)
obstruction of blood flow through the SVC
superior vena cava syndrome
What type of cancer is most common w/ SVC syndrome
adenocarcinoma of the right lung
- Most common symptom of SVC syndrome
- Other symptoms of SVC syndrome
- dyspnea (most common)
- other sxs: cough, chest pain, headache, head fullness, and facial swelling
chemo given before localized (surgical or radiation) treatment of cancer -> seeks to shrink tumor so that surgery many spare more normal tissue
neoadjuvant chemotherapy
chemo given after surgery with the goal of eliminating micrometastasis
adjuvant chemotherapy
the first lymph node to which cancer cells are most likely to spread from a primary tumor
sentinel node
4 tissue types affected by cancer treatment
mainly includes labile cells (continuous replication)- GI tract- bone marrow- hair and skin- reproductive tract
important factor in development of cancer -> causes cell mutation
chronic inflammation
Explain how cytokines can lead to cell mutation
cytokines are supposed to help the inflammatory process but when overproduced -> cause damage to tissues
Risk factor for cancers of the lung, lower urinary tract, upper aerodigestive, liver, kidney, pancreas, cervix, uterus, and myeloid leukemia
tobacco
What are some dietary sources of carcinogens?
- cooking fat, meat, or protein- naturally occurring carcinogens associated w/ plant food substances (alkaloids or mold byproducts)
What type of cancer are obese women at increased risk of and why?
breast cancer due to increased estrogen in their tissues
Risk factor for oral cavity, pharynx, larynx, esophagus, liver, colorectal, and breast cancers
alcohol consumption
What risk for cancer is dose related?
ionizing radiation
3 effects of UVA and UVB
- released TNF-a in epidermis- production of ROS- promotes skin inflammation and release of free radicals
3 types of skin cancer
- basal cell carcinoma (BCC)- squamous cell carcinoma (SCC)- melanoma (melanocytes)
incidence of BCC and SCC strongly correlate with what?
lifetime sunlight exposure
EBV is linked to what types of cancers?
nasopharynx and Hodgkin's and non-Hodgkin's lymphoma
6 types of cancers associated w/ HPV
- cervix- penis- vulva- anus- oropharynx (tongue and tonsils)
outdoor pollution is associated with what type of cancer?
lung cancer
3 main factors that lead to altered epigenomic marks
- lifestyle- carcinogen exposures- occupational exposures
What is ECF composed of?
- interstitial fluid (spaces between cells)- intravascular- lymphatics- transcellular (joint, intraocular, and CSF)
Describe whether each electrolyte is found more in ICF or ECF- Na- Cl- Ca- K- Mg
- Na = ECF- Cl = ECF- Ca = ECF- K = ICF- Mg = ICF
Name 4 factors in the absorption of fluid
- ADH- RAAS- ANP- renal function
What primarily regulates water balance?
antidiuretic hormone (ADH); aka vasopressin
What is another method the body uses to raise fluid volume or decrease plasma osmolarity other than ADH?
thirst -> increase fluid intake
Describe the RAAS system
decreased renal perfusion (decreased plasma volume) -> renin secreted -> Ang I -> Ang II -> ADH (water absorption) and Aldosterone (salt reabsorption) -> increased blood volume
What secretes renin and when?
juxtaglomerular cells when BP is low
What releases aldosterone and what stimulates it release?
released from the adrenal cortex; stimulated by Ang II or directly by increased plasma K
What causes production of ANP and BNP? What will ANP/BNP do?
- caused by cardiac distention (ECF volume increased, Na and H2O retention, increased BP)
- decrease RAAS - increase GFR - increase Na and water excretion (natriuresis and diuresis) - vasodilation (decrease BP)
3 lab tests used to measure renal function
- GFR- serum creatinine- serum BUN
What is the minimum normal urine output?
30 mL/hr
Normal blood osmolarity
275-295 mosm/Kg
What is responsible for the ECF water balance
Na
What will isotonic IV solution do? Ex. of isotonic solution
- remain in vessels -> add to blood volume
- 0.9% NaCl solution
What will hypertonic IV solution do? Ex. of hypertonic solution
- contains high Na -> will pull fluid from cells into vessels (useful in cerebral edema)
- 3-5% normal saline
What will hypotonic IV solution do?
- contains low Na -> fluid will be pulled into the tissues from the vessels
- 0.45% normal saline
Pathophysiology of edema (3)
- increased capillary permeability (proteins moves to interstitial space)- low levels of serum proteins- hydrostatic pressures increased due to venous obstruction, Na or water retention
Non-pitting vs pitting edema
- Non-pitting: swollen cells due to increased ICF volume- Pitting: increased interstitial fluid volume
T/F: A loss or gain of saline affects the volume of both ICF and ECF
False; saline is confined to the extracellular compartment -> does not affect volume of the intracellular compartment
Clinical presentation of isotonic fluid loss
- orthostatic hypotension- tachycardia- weight loss- decreased skin turgor and slow capillary refill- low urine output- hypovolemic shock
Clinical presentation of isotonic fluid excess
- hypertension - weight gain- edema- signs of CHF- may have increased urine output
Cause of hyponatremia
- excessive hypotonic IV- excess water intake (includes psychogenic polydipsia, tap water enemas, and NG irrigation)- vomiting/diarrhea- fresh water drowning- SIADH
What will happen to serum Na and cells with hyponatremia?
low serum Na and cellular swelling
Clinical presentation of hyponatremia and why?
- confusion, lethargy, coma- headache, weight gain- nausea- seizure, weakness, muscle twitching- decrease in Na concentration changes the cell's ability to depolarize and repolarize normally -> alters APs of neurons and muscles- will also see cerebral edema (causes many neurological changes)
Most important way to determine if someone is retaining fluid or losing fluid
Daily weights
Normal Na level
135-145 mEq/L
Causes of hypernatremia
- chronic diarrhea, vomiting and fever (water loss)- no access to water (decreased thirst)- diabetes insipidus- drowning in salt water- tube feedings- diaphoresis and diuresis- primary hyperladosteronism- Cushing syndrome
clinical manifestations of hypernatremia and why?
- confusion, lethargy, coma- seizure- fever- dry mucous membranes- hyperreflexia- pulmonary edema- CNS signs due to brain cells shrinking and Na can't cross BBB; also due to alterations in membrane potential
normal K levels
3.5-5.0 mEq/L
4 factors that enhance cellular uptake of K
- insulin- epinephrine- aldosterone- alkalosis (K is lo)
4 factors that enhance K release
- acidosis (H+ takes over cells)- cell lysis- strenuous excersice- increased ECF osmolarity
causes of hyperkalemia
- excess K intake- diuretics- large blood transfusions- decreased renal excretion- Addison's disease (decreased aldosterone)- crush injuries and burns (cell lysis)
Clinical signs of hyperkalemia
- muscle weakness/paralysis - cardiac dysrhythmias/arrest - hypopolarization (lowering) of RMP (easier to excite) - anxiety, numbness/tingling, N/V/D - tall, peaked, T wave
Causes of hypokalemia
- anorexia or NPO- diuretics- V/D- NG suction- intestinal drainage
Clinical signs of hypokalemia
- hyperpolarization (increasing) of RMP- muscle weakness/paralysis- paralytic ileus- dysrhythmias
Normal total Ca level
9-11 mg/dL
Normal ionized Ca level
4.5-6 mEq/L
Causes of hypercalcemia
- hyperparathyroidism (increased PTH secretion)- immobilization (stimulation breakdown of bones)- leukemia- diuretics
Clinical signs of hypercalcemia
- weakness and CNS depression- decreased NM excitability
Causes of hypocalcemia
- dietary deficiency (vitamin D)- laxative abuse- diarrhea- pancreatitis- malabsorption
Clinical signs of hypocalcemia
- cramps and seizures - increased NM excitability - low T wave
What is trousseau sign
- identifies hypocalcemia- inflate BP cuff on arm and will see flexion at wrist (carpal spasm)
What is Chovstek sign
- identifies hypocalcemia- tap the facial nerve anterior to the ear to elicit ipsilateral facial contraction
Normal Mg level
1.5-2.5 mEq/L
causes of hypermagnesemia
laxatives and antacids
Clinical signs of hypermagnesemia
- decreased reflexes- muscle weakness- drowsiness- respiratory depression- cardiac arrhythmias
causes of hypomagnesemia
alcoholism, poor nutrition, and malabsorption
Clinical signs of hypomagnesemia
- muscle cramps/spasm- tetany- seizures- hyperactive reflexes- cardiac arrhythmias
Normal Pi levels
2.5-4.5 mg/dL
causes of hypophosphatemia
- alcoholism- malabsorption- diarrhea- DKA- diuretics- antacids- dialysis
Clinical signs of hypophosphatemia
- anorexia- malaise- paresthesias- muscle weakness- decreased reflexes- confusion- impaired cardiac function
causes of hyperphosphatemia
- phosphate containing enemas- crushing injury- adrenal insufficiency- hypoparathyroid disease
Clinical signs of hyperphosphatemia
- increased NM excitability- Ca deposits in body tissues- hypocalcemia
Which electrolyte imbalances will cause weakness/poor muscle tone?
- hyperkalemia- hypokalemia- hypercalcemia- hypermagnesemia
Which electrolyte imbalances will cause twitchy/crampy muscles?
- hypocalcemia- hypomagnesemia
Normal blood pH
7.35-7.45
Normal blood PaCO2
35-45 mmHg
Normal blood HCO3 (bicarb)
22-26 mEq/L
causes of metabolic acidosis
- loss of base or addition of acid- DKA- lactic acidosis- EtOH poisoning
What is the compensation of metabolic acidosis?
hyperventilation (respiratory compensation) -> excrete more CO2
Clinical presentation of metabolic acidosis
- N/V/D- confusion/coma- Kussmaul breathing (deep and rapid)
causes of metabolic alkalosis
- addition of base or loss of acid- vomiting (loss of acid)- antacid tablets (gain HCO3)- diuretics (volume contraction)
What is the compensation of metabolic alkalosis?
hypoventilation (respiratory compensation) -> retain more CO2
Clinical presentation of metabolic alkalosis
- increased NM irritability- tetany- seizures- confusion- lethargy- coma
Respiratory acidosis compensation
decreased ventilation -> CO2 goes up -> kidneys increase HCO2 regeneration and acid excretion
causes of respiratory acidosis
CNS depression, airway obstruction, pneumonia, PE, COPD
Clinical presentation of respiratory acidosis
- headache- lethargy- confusion- tremors/seizures- cardiac arrhythmias
Respiratory alkalosis cause and compensation
increased ventilation (hyperventilation) -> CO2 decreases -> kidneys decrease acid excretion
Clinical presentation of respiratory alkalosis
- diaphoresis- NM irritability- carpopedal spasms- tingling around fingers/mouth- seizures/coma
What is the relationship between calcium and phosphate?
extracellular concentrations are inversely related -> both regulated by the same hormones
5 patterns of neurologic function that are critical to evaluate
- level of consciousness- pattern of breathing- pupillary reaction- oculomotor responses- motor responses
Explain the rhythm of Cheyne-Stokes respiration
- increased levels of CO2 -> tachypnea- CO2 levels decrease -> leads to apnea until CO2 accumulates again
4 criteria for brain death
- unresponsive coma (no motor or reflex movements)- no spontaneous respiration (apnea)- no brainstem functions (dilated, fixed pupils; no gag or corneal reflexes)- isoelectric EEG
death of the cerebral hemispheres exclusive of the brain stem and cerebellum (no behavior or environmental responses but brain can maintain homeostasis)
Cerebral death (irreversible coma)
complete unawareness of the self or surrounding environment and complete loss of cognitive function; can be seen in survivors of cerebral death
persistent vegetative state (VS)
sleep-wake cycle are present, eyes open spontaneously, and BP and breathing are maintained without support; brainstem reflexes intact but cerebral function lost
persistent vegetative state (VS)
individuals may follow simple commands, manipulate objects, gesture or give yes/no responses, have intelligible speech, and have movements such as blinking/smiling
minimally conscious state (MCS)
defect of pattern recognition -> failure to recognize the form and nature of objects (can be tactile, visual, or auditory)
Agnosia
agnosia is commonly associated w/ what neurological problem
CVA
Broca vs Wernicke
- Broca's area: helps in producing coherent speech- Wernicke's area: helps in speech processing and understanding language
acquired mental disorder characterized by deficits in attention and coherence of thought and action; secondary to intoxication, metabolic disorders, or nervous system disorders
acute confusional states (ACS); may also be called delirium
progressive deterioration of cerebral functions due to neurofibrillary tangles and plaques -> lead to neuronal death and brain atrophy
Alzheimer's disease (AD)
state of continuous seizures lasting more than 5 minutes or rapidly recurring seizure before the person has regained consciousness
status epilepticus
normal ICP
5-15 mmHg
causes of increased intracranial pressure (IICP)
increased intracranial content- tumor growth- edema- excessive CSF- hemorrhage
ICP may not change in this stage due to compensatory mechanisms
Stage 1 IICP
stage with continued expansion of intracranial contents and pressure may compromise neuronal oxygenation and systemic arterial vasoconstriction may occur to overcome IICP
Stage 2 IICP
Clinical manifestations of stage 2 IICP
subtle and transient - confusion- restlessness- drowsiness- slight pupillary and breathing changes
stage where ICP begins to reach arterial pressure and brain tissues experience hypoxia and hypercapnia -> rapid deterioration
Stage 3 IICP
Clinical manifestations of stage 3 IICP
- decreased levels of arousal- widened pulse pressure (systolic increases)- bradycardia- small, sluggish pupils
stage of IICP where brain tissue herniates from compartment of greater pressure to compartment w/ less pressure -> blood supply compromised -> further hypoxia in herniated tissues
Stage 4 IICP
Clinical manifestations of stage 4 IICP
- progression to deep coma- ipsilateral dilation and fixation of pupils -> bilateral dilation and fixation of pupils- abnormal breathing (Cheyne-stokes, ataxic, or central neurogenic hyperventilation)- pulse pressure begins to decrease (as brain herniates and ICP decreases)- pulse slightly irregular
At what stage of IICP is surgical or medical intervention the best?
Stage 2 IICP
Cause of hydrocephalus
interference of CSF flow- decreased reabsorption- increased production- obstruction within ventricular system
NT necessary to make muscle tone smooth
dopamine
AD hereditary degenerative disorder that causes severe degeneration of basal ganglia and frontal cerebral atrophy -> depletion of basal ganglia GABA (inhibitory NT)
Huntington disease (HD or Chorea)
severe degeneration of basal ganglia involving dopaminergic nigrostriatal pathway -> dopamine deficiency (inhibitory NT) and unopposed cholinergic activity (promotes muscle tone)
Parkinson disease (PD)
Classic manifestations of PD
- resting tremor- rigidity- bradykinesia/akinesia- postural disturbance (stooped)- short shuffling steps- cognitive-affective symptoms
Diagnostic hallmark of PD? What does it lead to later in disease?
- Lewy body formation in neurons (protein misfolding and accumulation of alpha-synuclein)- Lewy body dementia later in disease
temporary loss of all spinal cord functions below the lesion
spinal shock
neurodegenerative disorder that diffusely affects upper and lower motor neurons of the cerebral cortex, brain stem, and spinal cord (corticospinal tracts and anterior roots)
amyotrophic lateral sclerosis (ALS or Lou Gehrig disease)
Clinical manifestation of ALS
progressive muscle weakness leading to respiratory failure and death; pt has normal intellectual and sensory function until death
posture/response characterized by upper extremities flexed (held close to body) and lower extremities that are externally rotated and extended; occurs when the brainstem is not inhibited by the cerebral cortex motor area
decorticate posture/response
posture/response characterized by increased tone in extensor muscles and trunk muscles w/ active tonic neck reflexes (head is neutral and all 4 extremities are rigidly extended); caused by severe injury to the brain/brainstem
decerebrate posture/response
broad-based gait where person walks in small steps and the head and body are flexed -> due to basal ganglion dysfunction and seen in Parkinson disease
basal ganglion gait
exaggerated emotional response; excessive crying (left hemisphere) or laughing (right hemisphere); may not be appropriate to environment
hypermimesis
loss of emotional language (aprosody); inability to understand emotional in speech and facial expression or inability to express emotion
hypomimesis
brain injury at the site of impact
coup injury
injury from the brain rebounding and hitting opposite side of skull after impact
contrecoup injury
fracture at the base of the skull; pts can leak spinal fluid from their ears/nose and have raccoon eyes
basilar skull fracture
4 types of vertebral injuries
- simple fracture- compressed fracture (wedge; vertebral body compressed anteriorly)- comminuted fracture (vertebral body shattered into several fragments)- dislocation
normal activity of the spinal cord ceases at and below the level of injury due to lack of continuous nervous discharges from the brain; transient
spinal shock
causes of spinal shock
presence of hemorrhage or edema at the spinal cord; also due to transection of the cord which would not be transient
clinical manifestation of spinal shock
complete loss of reflex function (skeletal, bladder, bowel, sexual function, thermal control, and autonomic control) below level of lesion
syndrome of sudden, massive reflex sympathetic discharge associated w/ spinal cord injury at T6 or above where descending inhibition is blocked
autonomic hyperreflexia (dysreflexia)
Explain the cause of autonomic dysreflexia
- sensory receptors below level of cord lesion are stimulated- intact autonomic nervous system reflexively responds -> increase BP (sympathetics)- baroreceptors in cerebral vessels, carotid sinus, and aorta sense HTN and stimulate parasympathetics- HR decreases but vessels don't dilate because efferent impulses can't pass through cord
most common causes of autonomic dysreflexia
distended bladder or rectum; also caused by pain receptors in the skin, penis, and uterus
in autonomic dysreflexia, stimulation of the sympathetic nervous system will cause what (4)?
- vasoconstriction- hypertension- skin pallor- pilomotor spasms (goosebumps)
in autonomic dysreflexia, what parasympathetic response will occur above lesion (4)?
- arterial dilation- flushed skin- headache - sweating
fracture of the lamina (usually in the lumbar region; L5) and it causes a separation between adjacent vertebrae
spondylolysis
secondary to spondylolysis; anterior displacement (sliding) of the inferior vertebral segment
spondylolisthesis
condition due to a compressed nerve in the spine that can cause pain, numbness, tingling, or weakness along the course of the nerve/dermatome
radiculopathy
arise from arterial occlusions caused by thrombi formation in arteries supplying the brain or intracranial vessels
thrombotic stroke
involves fragments that break from a thrombus formed outside the brain (usually heart, aorta, or common carotid)
embolic stroke
stroke usually caused by occlusion of a single, deep perforating artery that supplies small penetrating subcortical vessels; will have pure motor or sensory deficits
lacunar stroke
a mass of blood is formed as bleeding continues into the brain -> adjacent brain tissue is displaced and compressed -> causes ischemia, edema, IICP, and necrosis
hemorrhagic stroke
most common type of brain aneurysm that is usually due to congenital abnormalities in the arterial wall; occur in large intracranial vessels and will cause subarachnoid hemorrhage if ruptured
saccular (berry) aneurysms
aneurysm that results from diffuse arteriosclerotic changes and are found most commonly in the basilar arteries or terminal portions of the internal carotid arteries
fusiform (giant) aneurysms
acute febrile illness, usually of viral origin, with nervous system involvement
encephalitis
acquired inflammatory disease causing demyelination of the peripheral nerves w/ relative sparing of axons; acute onset w/ ascending motor paralysis that usually occurs after respiratory or GI infection
Guillain-Barre syndrome
chronic inflammatory disease involving degeneration of CNS myelin, scarring (sclerosis or plaque formation), and loss of axons
multiple sclerosis
chronic autoimmune disease where IgG antibodies are produced against ACh receptors -> block binding of ACh and decrease muscle contraction
myasthenia gravis
symptoms of myasthenia gravis
- weakness and fatigue- ptosis (drooping of eyelid)- diplopia- difficulty chewing
most common types of urinary calculi
- calcium oxalate or calcium phosphate- struvite - uric acid
What causes nephrolithiasis
- supersaturation of one or more salts- precipitation of a salt from liquid to solid state- growth into a stone via crystallization or aggregation
How are kidney stones evaluated?
- imaging studies determine location of stone (KUB/CT/IVP)- UA to analyze contents of stone
Treatment of kidney stone
- high fluid intake- decreased dietary intake of stone-forming substances- stone removal
benign encapsulated tumors located near the cortex of the kidney
renal adenoma
most common renal neoplasm
renal cell carcinoma (RCC)
symptoms are renal cancers
- usually no early symptoms- later sxs include gross, painless hematuria and dull, achy flank pain
most common metastasis sites of RCC
- lung- liver- bone- thyroid- CNS
most common bladder malignancy
transitional cell carcinoma
risk factors for RCC
- smoking- obesity- analgesic use
symptoms of acute cystitis
- urinary frequency- dysuria- urinary urgency- lower ABD pain and/or suprapubic pain
nonbacterial or noninfectious cystitis
interstitial cystitis
symptoms of interstitial cystitis
- bladder fullness- urinary frequency - small urine volume- chronic pelvic pain- dyspareunia
acute infection of the renal pelvis and interstitium; most common cause is vesicoureteral reflux; associated w/ E. coli, proteus, and pseudomonas
acute pyelonephritis
symptoms of pyelonephritis
- fever/chills- flank or groin pain- other symptoms characteristic of a UTI
Common causes of glomerulonephritis
- type II, III, or IV hypersensitivity- drugs or toxins- vascular disorders (vasculitis)- systemic disorders (DM- post-strep infection
most common cause of end-stage renal failure
glomerulonephritis
What lab work will be seen w/ glomerular disease?
- decreased GFR- increased plasma creatinine and urea- reduced creatinine clearance
Explain how glomerular disorders can lead to edema
increased glomerular capillary permeability -> passage of plasma proteins into urine -> hypoalbuminemia -> decreased vessel oncotic pressure and fluid moves into interstitial space -> edema
excretion of 3.5 g or more of protein in the urine per day; due to glomerular injury
nephrotic syndrome
clinical manifestations of nephrotic syndrome
- hypoalbuminemia -> edema- hyperlipidemia and lipiduria (low albumin stimulates lipoprotein synthesis by liver)- vitamin D deficiency (decreased D activation by kidneys)- proteinuria- microscopic hematuria and RBC casts
causes of decreased renal perfusion
- hypotension- hypovolemia (hemorrhage or fluid loss)- sepsis- inadequate cardiac output- renal artery stenosis
most common cause of intra renal kidney injury/failure
acute tubular necrosis (ATN)
urine output less than 400ml/day
oliguria
urine output less than 50 ml/day
anuria
Elevated levels of urea and other nitrogen compounds in the blood.
azotemia
Stage of CRF w/ normal kidney function (GFR >90 ml/min); HTN
stage 1 CRF
Stage of CRF w/ mild kidney damage (GFR 60-89 ml/min); possible elevation of BUN and creatinine and HTN
stage 2 CRF
Stage of CRF w/ moderate kidney damage (GFR 30-59 ml/min); mild w/ HTN
Stage 3 CRF
Stage of CRF w/ severe kidney damage (GFR 15-29 ml/min)
Stage 4 CRF
ESRF w/ GFR < 15 ml/min
Stage 5 CRF
symptoms of stage 4 and stage 5 CRF
- moderate HTN- EPO deficiency anemia- hyperphosphatemia and hyperkalemia- hyperlipidemia- metabolic acidosis- salt/water retention
systemic manifestations seen due to urea accumulation because of renal dysfunction
uremic syndrome/uremia
