Things I struggle with Flashcards
case control study
copmapre a group of people with the disease to a group without the disease to look for risk factor. Odds ratio
cohort study
takes a group of people with a risk or exposure to a group without an exposure to see if it increases frequency of disease. Use relative risk
Phase 1 clinical trial
is it safe
phase 2 clinical trial
does it work
phase 3 clinical trial
is it better
phase 4 clinical trial
long term issues
sensitivity
a/a+c proportion of people with disease that test positive for disease. In other words, if the disease is present, the test will be positive. It is good for ruling out disease and indicates low false native. It is good for screening low prevalence disease
specificity
d/D+B- proportion of all people without disease who test negative. Disease is not present if the test is negative. It is good for confirming a positive screening test. It is used to rule in a disease
PPV
probation of positive test results that are true positive. If person tests +then they have disease. Prevalence increases the value
NPV
If person tests negative then they don’t have the disease. High prevalence means the NPV decreases.
incidence
number of new cases/ people at risk
prevalence
number of cases/people in population
chronic disease- changes in incidence and prevalence
prevalence is greater than incidence because there is a larger number of existing cases
when does the odds ratio equal the risk ratio
if the prevalence is low
precision
consistence and reproducibility of the test
accuracy
trueness of the test measurements
reliability
precision
validity
accuracy
Beckson Bias
hospital patients are used instead of normal healthy control
recall bias
can remember more exposures if there is a disease present
Pygmalian effect
observer believes the treatment works so records a biased view
Procedure bias
groups are not treated the same
confounding bias
other multiple factors are playing in
Hawthorne effect
people change behavior when being watched
lead time bias
early detection does not mean increased survival time
1 std
68%
2 std
95%
3std
99.7%
for 95% CI what is z
1.96
for 99% CI what is z
2.58
type 1 error
false positive
type 2 error
false negative- can be influenced by number of participants
beneficience
act in best interest of the patient
non-maleficence
do not harm
exceptions for informed consent
emergency, legally incompetent, witholding psychiatric records, waiver
minor can concept for
sex, drugs, and rock n roll
order of surrogates
spouse>adult children>parents>adult siblings>other relatives
does a proxy come first or spouse in decisions
proxy
transference
patient projects feelings about formative or other important figures onto the physician. Psychiatrist is seen as a parent to the patient
countertransference
doctor projects feelings about people onto the patient.
fixation
partially remaining at a childsih level of development- like focussing on video games
idealization
expressing extremely positive thoughts of self and others while ignoring negative thoughts
identification
modeling behavior after another person who is more powerful- abused child becomes abuser
intellectualization
using factors of logic to emotionally distance oneself
isolation of affect
separating feelings from ideas and events
projection
attributing an unacceptable internal impulse to an expernal source- husband thinks wife is cheating because he is cheating
displacement
transferring avoided ideas and feelings to a neutral person- mother yells at child because husband yelled at her
reaction formation
replacing a warded off idea or feeling by an emphasis on the opposite
repression
involuntarily withholding an idea or feeling from conscious awareness
sublimation
replacing unacceptable wish with a course of action that does not conflict with values
suppression-
intentionally holding off worry
Tourettes
before 18 with sudden rapid recurrent stereotypes motor and vocal tics for over 1 year. associated with OCD and ADHD. Can treat with antipsychotics or tetrabenazeine, guanfacine, and clonidine
positive symptoms of schizo
delusions, hallucinations, disorganized speech, disorganized or catatonic behavior,
negative symptoms of schizo
affective flattening, avolition, anhedonia, asociality, alogia
tuboinfundibular pathway
increased prolactin secretion from schizo treatment
nigrostriatal pathway
EPS effects
mesocortical pathway
negative symptoms
mesolimibic pathway
positive symptoms
brief psychotic disorder vs. schizophreniform
brief is 1 month, and schizophreniform is 1-6 months
schizoaffective
two weeks of hallucinations or delusions without a major mood episode plus periods of concurrent major mood episode and schizophrenia
pathologic grief
persistent and causes functional impairment. meets criteria for major depression
adjustment disorder
emotional symptoms or anxiety or depression causing impairment following an identifiable psychosocial stressor and lasting under six months or over 6 months in the proscenia of a chronic stressor
PTSD
exposure to prior trauma, intrusive re-experiencing of the event, avoid stimuli, changes in cognition and mood and persistently increased arousal- lasts over 1 month with significant distress or dysfunction
somatic symptom disorder
variety of body complaints lasting for months to years associated with excessive persistent thoughts and anxiety about symptoms. May co-occur with medical illness
conversion disorder
loss of sensory or motor function often from an acute stressor. Patient is aware of but indifferent toward symptoms.
illness anxiety disorder
excessive preoccupation with acquiring or having a serious illness despite medical evaluation and reassurance; minimal somatic symptoms
what is decreased in narcolepsy
hypocretin/orexin production
precontemplation
not acknowledging there is a problem
contemplation
acknowledging that there is a problem but not be willing yet to make a change
alcohol withdrawal
tremor, autonomic hyperactivity, seizures
opioid withdrawal
sweating, dilated pupils, piloerection, fever, rhinorrhea, yawning, nausea, stomach cramps, diarrhea
barbituate withdrawal
delirum and life threatening cardiac collapse
bezo withdrawal
sleep disturbance, depression, rebound anxiety, seizure
stimulant withdrawal
post use crash, depression, lethargy, increased appetite, sleep disturbance and vivid nightmares
what can you treat cocaine overdose with and what will kill them if you give them
treat with alpha blockers and benzos. If you give a beta blocker, you get increased hypertension because there is uncontrolled alpha stimulation
violence, impulsive, psychomotor agitation, nystagmus, tachycardia, hypertension, analgesia, psychodis, delirium, seizures
PCP- treat with antipsychotic or benzo
perceptual distortion, depersonalization, anxiety, flashbacks, paranoia,
LSD
euophoria, delusions, anxiety, paned, perception of time is slowed, social withdrawal, hallucinations, red eyes,
weed
irritable, anxiety, depression, insomnia, restlessness, and decreased appetite
pot withdrawal
delerium tremens
autonomic hyperactivity, tremors, anxiety, seizures, seen after surgery because cannot be drinking. hallucinations 12-48 hours after last drink
neuroleptic malignant syndrome
rigidity, myoglobinuria, autonimic instability, hypyrexia- treat with dantrolene, or bromocriptine to get the D2 flowing again
what is in the follicle of a LN
B cells maturation and germinal centers
what is in the medulla of a LN
plasma cells
what is in the paracortex of the LN
T cell
what makes the paracortex of the LN hypoplastic
Digeorge
what makes the paracrotex of the LN hyperplastic
viral infections
what happens after a splencectomy and why
decreased IgM, decreased complement activation, decreased C3b opsonization, and increased susceptibility to encapsulated organisms
what cells are seen after a splenectomy
Howell Jolly bodies, target cells, thrombocyotsis from loss of sequestration, lymphocytosis
what is the thymus derived from
third pouch
when the thymus hypoplastic
Digeorge and SCID
when is the thymus hyperplastic
Myasthenia Gravis
adaptive immunity
T and B cells, highly specific and used immunoglobulin. memory cells cause quicker response the second time
innate immunity
neurophils, macrophages, monocytes, complement- rapid and CRP and TLR bind PAMP
MHC I
binds TCR and Cd8, and is on all nucleated cells. It presents cytosolic proteins or antigens to the CD8 cells
MHC II
binds TCR and CD4 cells. These are only on APC cells. It presents exogenous proteins like bacterial proteins to the T helper cells to activate them
what enhances the activity of NK cells
IL2, IL12, IFNalpha, IFN beta
positive selection of T cells
has TCR that can bind the self-MHC- this occurs in the cortex
negative selection of T cells
eliminate TCRs that bind the self antigen on the dendritic cells or thymic medullary cells. This is the elimination of autoimmune cells- occurs in the medulla
Th1 cells activation
It is induce by IFN gamma and IL12 to secrete IFN gamma which activates the macrophages and the cytotoxic T cells. It is inhibited by IL4 and IL10
Th2 cells activation
induced to differentiate by IL4 and they secrete IL4, IL5, IL10, IL13 which recruit eosinophila for parasite defense and promote IgE production by B cells. It is inhibited by IFN gamma
what does hepcidin do
it decreases iron absorption by degrading ferroportin and decreases iron release from macrophages and leads to anemia of chronic disease
what does CRP do
it is an opsonin which fixes complement and facilitates phagocytosis. Measured clinically as a sign of ongoing inflammation
what mediates the classic complement pathway
IgG and IgM
what are the opsonins
C3b and IgG are the two first degree ones which enhance phagocytosis. They coat cells so the Fc ro C3B receptors can grab onto them
what is the function of C1 esterase inhibitors
it prevents complement activation on self cells
C1esterase inhibitor deficiency
causes hereditary angioedmea due to unregulated activation of chalkier and increased bradykinin. ACE inhibitors make it worse. There is facial swelling, laryngeal swelling and GI issues
C3 deficiency
increases risk of severe recurrent pyogenic sinus and respiratory tract infections and increased susceptibility to HN3
C5-C9 deficiency
leads to Neisseria infections repeatedly
DAF deficiency
complement mediated lysis of RBCs and paraoxysmal nocturnal hemoglobinuria
what cytokine causes fever and acute inflammation- activates endothelium to express adhesion molecules and induces chemokine secretion to recruit WBC
IL-1
what cytokine causes fever and stimulates production of acute phase proteins
IL-6
what cytokine is the major chemotactic factor for neutrophils
IL-8
what cytokine induces differentiation of T cells into Th1 cells. Activates NK cells
IL12
what cytokine mediates septic shock, activates endothelium and causes WBC recruitment and vascular leak
TNF alpha
what cytokine stimulates growth of T helper, cytotoxic, and regulatory T cells and NK cells
IL2
what cytokine supports growth and differenctiaon of bone marrow stem cells
IL3
what cytokine is secreted by NK cells and T cells in response to IL12 from macrophages and stimulates macrophages to kill phagocytes pathogens. Inhibits differentiation of TH2 cells
interferon gamma
what cytokine induces differentiation of T cells into TH2 cells. Promotes growth of B cells and enhances class switching to IgE and IgG
IL4
what cytokine promotes growth and differentiation of B cells and enhances IgA and stimulates growth of eosinophiles
IL5
What cytokine attenuates inflammatory response. Decreases expression of MHCII and Th1 cytokines. Inhibits activates macrophages and dendritic cells. Also secreted by regulatory T cells
IL10
what cytokines are secreted by macrophages
IL1, 6, 8, 12, and TNF alpha
what cytokines are secreted by all T cells
IL2 and IL3
what cytokines are secreted from Th1 cells
interferon gamma
what cytokines are secreted from Th2 cells
Il-4, 5, 10
why is sputum blue green
myeloperoxidase
what are the first two steps in the respiratory burst
NAPH oxidase and superoxide dismutase
what does NADPH do
generates the ROS
what does superoxide dismutase do
produces H2O2
what is the deficiency in with chronic granulomatous disease and what are the risks
increased granuloma formation because there are increased infections from catalase positive species which are able to break down the H2O2 from superoxide dismutase. The ROS are not generated because of the lack of NADPH disputes. Increased s aureus and aspergillus
what are interferons
they are glycoproteins secreted by virally infected cells that prime the uninfected cells which help them degrade factors the virus needs for replication
CD3, CD28, B7, CXCR4, CCR5
T cells
CD4 and CD40L
Helper T cells
CD8, CXCR4, CCR5
Cytotoxic T cells
CD19, CD20, CD21, CD40, MHCII B7
B cells
what receptor binds EBV
CD21
CD14, CCR5, MHCII, B7, Fc, C3b
macrophages
CD16 CD56
NK cells
CD34
hematopoetic stem cells
what are the antigen presenting cells
macrophages, B cells, dendritic cells
what kind of immune response do you get from a live attenuated vaccine and which vaccines are live
indue cellular and humoral responses. nasal flu, measles, mumps, polio (sabin), rubella, varicella, yellow fever
what live vaccines can you give to AIDS patients
yellow, MMR, varicella
what kind of response does killed vaccines give and which are killed
induce only a humoral response which may require a booster. Rabies, flue, polio salk, hepatitis A
anaphylactic atopic, IgE crosslinks on mast cells triggering immediate release of vasoactive amines, that react with post capillary venues. Reaction develops rapidly after antigen exposure because of preformed antibody. Delayed reopens follows due to production of arachidonic acid and metabolites
Type 1 HSN
rhinitis, hay fever, eczema, hives, asthma
HSN1
anaphylaxis
HSN1
IgM and IgG mediated that bind to a fixed antigen on a cell and does cellular destruction by opsonization, phagocytosis, complement and Fc medicated inflammation, antibody mediated cellular dysfunction
HSN2
Direct Coombs
detects antibodies that have adhered to patients RBC
indirect coombs
deterects antibodies in the serum that adhere to other RBC
widespread thrombosis of graft vessel with ischemia and necroses- graft must be removed- why did it happen and what kind of rejection is it
pre-existing antibodies react to donor antigen, and activate complement- hyperacute
Proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fbrosis- atheroscleosis
CD4 T cells respond to recipient APC presneintg donor peptides including allogenic MHC. Type I and IV sensitivity- chronic
bronchiolitis obliterans- dyspnea, dry cough, wheezes
chronic
vasculitis of graft vessels with dense interstitial infiltrate. CD8 cells activated against donor MHC HSN4.
acute-
accelerated atheroscelorisis after transplant
chronic
Increased HTN and CA, with fibrosis and internal thickening, mononuclear infiltrate with tubular atrophy and interstitial firbrosis- after transplant
chronic
vanishing bile ducts- transplant
chronic
maculopapular rash, jaundice, diarrhea, heaptosplenomegaly
gradted immunocomputent T cells proliferate in the immunocomprimised host and reject host cells with foreign proteins- type IV HSN- graft vs host- only happens in liver and bone marrow
intrinsic apoptosis
Bcl2 is anti-apoptotic and BAX or BAK is pro-apoptotic. If BCL2 is overexposed then the cells won’t die
extrinsic apoptosis
Fas ligand or TNF alpha. Immune cells with perforin and granzyme
coagulative necrosis
heart- ischmia or infarct in most tissue but the brain
liquefactive necrosis
bacterial abscesses, brain infarcts due to increased fat content. Neurtrophils release lysosomal enzymes that digest the tissue. Microglia test to be first. Early is cellular debris and macrophages and then its cavitation and cavitation
caseous necrosis
TB, systemic fungi- macrophages wall off the infecting microorganism- granular debris- fragmented cells and debris surround. This leads to cottage cheese appearance
Fat necrosis
enzymatic- acute pancreatitis saponification of peripancreatice fat or breast trauma- outilines of dead fat cells without nuceli- appears dark blue of H and E stain
fibrinoid necrosis
immune reaction in the vessels- immune complexes combine with fibrin and vessel wall damage- vessel walls are thick and pink
gangrenous necrosis
distal extremity after chronic ischemia- dry is ischemia and wet has a superfinection
reversible signs of cell injury
cellular and mitochondrial swelling, nuclear chromatin clumping, membrane blebbing,
irreversible cell injury
mitochondrial permeability and vacuolization, nuclear pyknosis- condensation, karyolysis which is fading and plasma membrane damage and lysosomal rupture
areas first hit by ischemia in brain
ACA/MCA/PCA
areas first hit by ischemia in heart
sunendocardium
areas first hit by ischemia in kidney
PCT
areas first hit by ischemia in liver
area around central vein
areas first hit by ischemia in colon
splenic flexure and rectum
red infarct
occur in venous occlusion and in tissues with multiple blood supplies like liver, lung, intestine, testes, reperfusion
what causes re-perfusion injury
the free radical damage
pale infarct
occur in solid organs with a single blood supply like the heart, kidney, and spleen
chromatolysis
neuronal axonal cell injury- there is increased protein synthesis in effort to repair famed axon- round cellular swelling, displacement of nucleus, dispersion of Nissle substance and Wallerian degeneration
dystrophic calcification
ca desposit in abnormal tisseus due to necrosis or injury- tends to be localized. No abnormal calcium level
metastatic calcification
widespread diffuse deposition of CA. Can be high calcium levels. Tend to be in interstitial issues.
chemotaxtic agents for neutrophils
C5a, IL8, LTB4, kalikreinin, platelet activating factor
what provides the strength to a scar
collagen
keloid- why does it happen
PDGF and TGF beta are controlling fibroblast growth and proliferation. TGF beta stimulates CT synthesis and remodelling in the extracellular matrix. TGF beta tends to decrease in maturation place to limit collagenase. Increased TGF beta from this
PDGF
secreted by platelets and macrophages. Induces vascular remodeling and smooth muscle cell migration stimulates fibroblast growth factor for collagen synthesis
proliferative phase of wound- up to 3 weeks
deposition of granulation tissue and type II collagen. Angiogenesis, epithelial cell proliferation, dissolution of clot and wound contraction
remodeling phase of wound healing- 1 week- 6 months
type III collagen replaced by type collagen I and increased tensile strength
what leads to granuloma formation
IFN gamma and activation of TNF alpha from macrophages induces and maintains granuloma formation
exudate
cellular- cloudy, increased protein, increased LDH, and its from lymphatic obstruction, inflammation/infection, malignancy
transudate
hypocellular, decreased protein, decreased LDH, low specific gravity, increased hydrostatic pressure, decreased oncotic pressure
ESR- increased
products of inflammation coat RBCs and cause aggregation. The denser RBC aggregates fall at a faster rate within a pipette tube. Increased with anemia, infections, inflammation, cancer, renal disease, pregancny
decreased ESR
sickle cell, polycythemia, HF, mucrocytosis, hypofibrinogeninemia
amyloidosis
abnormal aggregation of proteins into beta pelted sheets damage and apoptosis. Apple green bipfringence
primary amyloidosis
deposition of proteins from Ig light chains. Can occur as plasma cell disorder or associated with multiple myeloma. It is restrictive cardiomyopathy, renal disease, hematologic, easy bruising, splenomegaly, hepatomegaly, neuropathy
lipofuscin
wear and tear pigment associated with normal aging. Formed by oxidation and polymerization of autophagocytosed organellar membranes. Autopsy of elderly person will reveal deposits in the heart, colon, liver, kidney, eye, and other organs
hypertrophy vs. Hyperplasia
hypertrophy is increased in size of cells. hyperplasia is the increase innumber of cells. Risk of future malignancy
metaplasia
replacement of one cell type by another. Usually due to exposure to an irritant such as gastric acid or cigaretter smoke. Can undergo malignant transformation if its not removed
neoplasia
uncontrolled clonal proliferation of cells can be benign or malignant
dysplasia
disorded non enoplastic ell growth used only with epithelial cells. Mild dysplasia is usually reversible, severe dysplasia can move onto carcinoma
anaplasia
loss of cell polarity, complete disruption of normal architecture, pleomorphic cells, large nucleus to cytoplasm rain, increased mitotic figures, giant multinucleated giant cells
cancer grade
degree of cellular differentiation and mitotic activity-
cancer stage
degree of localization spread based on site and size of spread to lymph nodes
alkylating agents
leukema and lymphoma
aromatic amines
transitional bladder cancer
aresnic
liver, lung, skin
carbon tetrachloride
liver
nitrosamines
stomach cancer
radon
lung cancer
vinyl chloride
liver cancer
Psammoma bodies in what cancers
papillary thyoid cancer, serous papillary cystadenocarcinomal of ovary, meningioma, malignant mesotheliuoma- dystrophic calcification
breast cancer screening
mammogram once every 2 years from 50-75 years
cervical cancer screening
21-65 and once every 3 years
lung cancer screening
CT annually if 30 year pack history
what amino acids are histones rich in and why
lysine and arginine- they are positively charged
what does histone acetylation do to the DNA
it makes it relaxed making the DNA active
difference between nucleoside and nucelotide
nuceloside is a base plus a sugar and a tide is a base plus ribose plus phosphate
what are the amino acids needed for purine synthesis
glycine, aspartate, and glutamine
what are the pureines
a and g
pyrimidines
C, U, T
what is the rate limiting step of pyrimidine synthesis
CPSII
what is the rate limiting step of purine synthesis
PRPP synthetase
what is the nitrogen source for pyrimidine synthesis
glutamine
increased orotic acid, no increase in ammonia, megaloblastic anemia- what is the deficient enzyme- what pathway is this a part of
UMP synthase and pyrimidine synthesis
what med blocks PRPP synthase
azothioprine/6 mercaptopurine
what enzyme degrades 6-MP and what can cause toxicity from this med
it is metabolized by xanthine oxidase and if also take allopurinol it can lead to toxic accumulation of 6mp
what enzyme takes IMP to GMP and what pathway is this in
It is in the purine denovo synthesis pathway and it is IMP dehydrogenase
what medication blocks the conversion of IMP to GMP aka what enzyme does it block and what is the medication used for
It blocks IMP dehydrogenase- mycophenolate and ribavirin prevents the synthesis of purines in B and T cells
what enzyme takes UDP to dUDP and what blocks it and what pathway is it a part of
It is ribonucelotide reductase and it is blocked by hydroxyurea which is used in Sickle cell to increase the production of fetal hemoglobin. It is part of the pyrimidine pathway
what enzyme takes dUMP to dTMP and what blocks it and what pathway is it a part of
it blocks thymidilate synthase. It is 5 flurouracil. It has increased action with leucovorin as compared to methotrexate. It needs folic acid to continue to blockade the production of pyrimidines
what enzyme recycles dihydrofolate to to tetrahydrofolate and what 2 things block this. What pathway is it a part of and what is the drug to rescue this pathway
tetrahydrofolate reductase is blocked by methotrexate and trimethoprim, and pyrimethamine- these are for humans, bacteria, and protozoa respectively. Leucovorin can rescue this pathway by providing an excess of folic acid
what is the point of the purine salvage pathway and what does it produce
it is a way to recycle purines once they are used. It produces uric acid
what enzyme converts hypoxanthine to xanthine and xanthine to uric acid. What medication blocks this transformation
It is xanthine oxidase which is targeted by allopurinol. Allopurinol and febuxostat decrease the production of uric acid which contributes to gout. Also allopurinol can decrease the metabolism of 6mp and azothioprine
what enzyme converts guanine to GMP and hypoxanthine to IMP
HGPRT
Child is aggressive, has increased uric acid, gout, is aggressive, dystonic, and has self-mutilation like lip biting and finger biting- what is the enzyme that is deficient and what pathway is it a part of- what is the treatment
HGPRT deficiency also called Lesch Nyhan syndrome- It cannot recycle purines, so there is an overproduction of uric acid and continuous denovo purine synthesis- It is treated with allopurinol to help decrease the uric acid production, but it can only really treat the gout
what enzyme takes adenosine to inosine
adenosine deaminase
child has failure to thrive, chronic diarrhea, thrush, and constant recurrent infections with opportunistic and any other infections. No thymic shadow, and no germinal centers on the LN and no migration of T cells in the candida skin test- what enzyme is deficient and what pathway is it a part of
adenosine deaminase deficiency causing SCID it is part of the purine salvage pathway
megaloblastic anemia that does not improve with folate or B12
orotic aciduria
unwinds DNA template at replication fork
helicase
prevents strands from re-anealing
single stranded binding proteins
create double or single stranded breaks in DNA helix to add or remove supercoils
DNA topoisomerase
what is another name for DNA topoisomerase II
gyrase
what blocks prokaryotic DNA topoisomerase II and IV and what is it used for
FQ used for antibiotic
what blocks eukaryotic topoisomerase II and what is it used for
etoposide and teniposide- these are used for leukemia and lymphoma
this is prokaryotic only and elongates the leading strand by adding deoxynucleotides to the 3’ end. Elongates the lagging strand until it reaches the end. what kind of proofreading does it have
it is DNA polymerase III and has 3’-5’ proofreading
This is a prokaryotic enzyme only and it degrades RNA primer and replaces it with DNA and what proofreading does it have
it is DNA polymerase I and it has 5’-3’ proofreading
eukaryotic and has primer and starts the synthesis
polymerase alpha
eukaryotic and has the job of repairing the DNA during replication
polymerase beta
eukaryotic and has the job of doing the lagging strand replication
polymerase delta
eukaryotic and has the job of replacing the leading strand
polymerase epsiolon
eukaryotic and has the job of replicating the mitochondrial DNA
polymerase gamma
catalyzes the formation between the Okasaki fragments
DNA ligase
a RNA dependent DNA polymerase that adds DNA to the 3’ end of chromosomes to avoid loss of genetic material with every duplication- only in eukaryotes
it is telomerase
what does transition mutation mean
purine to purine or pyrimidine to pyrimidine
what does transgression mutation mean
purine to pyrimidine or the other way around
what kind of mutation is a substitution of base but still codes for the same aa
silent mutation
what kind of mutation is a nucelotide substitution resulting in changed amino acid
missense mutation- sickle cell disease
what kind of mutation is a nucleotide substitution leading to an early stop codon
nonsense mutation
what kind of mutation is a deletion or inception of a number of nucleotides not divisible by three, resulting in misreading of all of the nucleotides downstream from the error. Protein may be shorter or longer rand can be disrupted or altered function
frameshift mutation
what kind of mutation is a retained intron in the mRNA leading to a protein with impaired function or altered function
it is a splice site mutation which can lead to cancer, dementia, epilepsy, and some types of beta thalassemia
what changes occur with low glucose on the lac operon site
increased adenylate cyclase activity which increases the cAMP generation from ATP and activates the catabolite activator protein and increased transcription
what changes occur with high lactose on the lac operon site
unbinds the repressor protein and increases the transcription
specific endonuclease release oligonucleotides containing damaged bases. DNA poly and ligase fill and reseal this gap. It repatriate bully and distorted lesions-
nucleotide excision repair
what is defective in xeroderma pigmentosum and what causes damage
defective endonuclease repair- removal of dimer and it is in nucleotide excision repair and it mutates in exposure to sunlight
base specificc glycosylase rmovesthe altered base and creates a base site without a purine or pyrimidine. And then it is filled in with beta polymerase
Base excision repair
new synthesized strand is recognized, mismatched nucleotides are removed and the gap is filled and resealed- occurs in G2 phase
Mismatch repair
what is deceptive in Lynch syndome
mismatch repair
brings two ends of DNA fragments together to repair double stranded breaks- not homologous- what is it called when this is defective
non homologous end joining- it is mutated in ataxia telangactase and Faconi anemia
what are the start codons
AUG which his methionine
what are the stop codons
UGA, UAA, UAG
what are the DNA binding motifs
zinc finger, helix loop helix, helix turn helixm and leucine zipper
how do you terminate prokaryotic RNA transcription
Rho factor knocks off RNA polymerase or a GC rich region self binds creating a hairpin loop which knocks off the polymerase
site where RNA polymerase II and multiple other TFs bid to DNA upstream from the gene- AT rich segment with TATA or CAAT and what would a mutation here do
promoter region and it would decrease the level of gene transcription
stretch of DNA that alters the gene expression by binding TFs
enhancer
site where negative regulators bind
silencer
what makes rRNA in eukaryotes
RNA poly I
what makes tRNA in eukaryotes
RNA poly III
what makes mRNA in eukaryotes
RNA poly II
what inhibits RNA polymerase II
amanita phalloides- death cap mushroom which causes severe hepatotoxicity
what drug inhibits RNA polymerase in prokaryotes and eukaryotes
rifampin
what processes occur in the nucleus after transcription
capping of the 5 prime end, polyadenylation of the trial, spline of the introns and this is the mRNA
what do p bodies do
they are processing bodies which are quality control of the mRNA in the cytoplasm
what do spliceosomes do
they move introns with GU at the 5’ end and AG at the 3’ stie mutations lead to inappropriate splicing and impaired function of the protein
what can cancer cells do with altered splicing to avoid apoptosis
they can alternatively splice to that Fas loses its transmembrane domain this means that it cannot be in the membrane, so that it cannot be bound.
what is at the end of the 3’ end of tRNA
it is the CCA end which carries the amino acid
what charges the tRNA
aminoacyl tRNA syntheses scrutinizes the amino acid before it binds to tRHA and it hydrolyzes and it in charge of the accuracy of the tRNA
what order are the RNA sites
APE: A is incoming and P is growing peptide and E is the exit site
what are the numbers of the eukaryotic and prokaryotic RNA
Euk- 40, 60, 80 and Pro are 30,50,70
what happens when Rb is hypophosphorylated
it is active then so it binds E2F to prevent the progression of G1 to S phase
what role does P53 play in the cell cycle
it checks at G1 to S and G2 to M to make sure there is not too much damage. if there is it cannot be used and causes cell to degrade
dyenin goes which way
retrograde
chines goes which way
anterograde
what drugs act on microtubules
mebensazole, griseofulvin, colchicine, vincristen and blastine which stop growth, and paclitaxel whch stabalizes
infertilty, increased ectopic pregnancy, bronchiectasis, recurrent sinusitis, and situs inverses or dextrocardia on the CXR- what is the disorder and why
Kartagener syndrome and it is from defect in dynein arm, so cilia do not move
collagen found in cartilage, vitreous body, and nucleus pulposis
collagen II
collagen in bone, skin, tension, dentin, fascia, and cornea with late wound repair
type I
collagen found in the basement membrane, basal lamina, and lens
Type IV
collagen found in skin, blood vessels, uterus, fetal tissue and granulation tissue
Type III
OI is associated with which collagen
type I collagen
vascular Ehlers Danlos is associated with which type of collagen
Type III
Alport and Goodpasture involve which collage
Type IV
many fractures wit little trauma, blue sclerae, hearing loss and tooth acbomalities- types of it
abnormal collagen I. It is fatal in type II
hyper extensible skin and hyperbole joints. what type of collage in the this kind. what kind of collagen is the vascular kind and what is the defieincy
type V is the normal kind. vessel is III collagen. It can be a deficiency in the lys oxidase which forms the bonds between tropocollagen. or a deficiency in pro collagen with peptidase enzymes
what aa are the elastin rich in
proline, glycine and lysine
Marfan is a defect in what
fibrillin which is the glycoprotein that forms the sheath around the elastin
what are wrinkles from
decreased collagen and elastin production
what causes panacinar emphysema
overactive elastase because there is not enough alpha 1 antitrypsin blocking it
test used to amplify a DNA fragment
PCR
Blot that looks for mutated DNA
southern blot
blot that looks at RNA for the levels of mRNA which is reflective of gene expression
Northern blot
sample protein is separated by get electrophoresis and transferred to a membrane and label is used to bind a relevant protein. Shows that transcription is increased
western blot
identifies DNA binding proteins aka transcriptin factors using labelled probes
southwestern blot
known antibody to test for presence of antigen
direct ELISA
known antigen to test for antibody
indirect ELISA
ohenotype varies among individuals with the same genotype
variable expressivity
one gene contributes to multiple phenotypic effects
pleiotropy
increased severity with earlier onset of disease in succeeding generations
anticipation
mutations in different loci can produce a similar phenotype
locus heterogeneity
different mutations in the same loci produce the same phenotype
allelic heterogeneity
both normal and mutated tDNA resulting in variable expression in mitochronidrally inherited disease
heteroplasmy
only one allele is alive and the other is inactive with one allele inactivated deletion of the active allele disease. Methylation picks one parent to express the gene
imprinting
maternal imprinting and gene from mom is normally silent but paternal gene is deleted or mutated or there is maternal disomy- hyperphaia, obesity, intellectual disability, hypogonadism, and hypotonia
Prader Wili
dads gene is usually silent but maternal is deleted or mutated. Or parental disomy- it has laughter, seizures, ataxia, and severe intelletual disability
Angelman syndrome
bilateral massive enlargement of kidney dues to large cucsts. mutation in PKD1 with berry aneurysms
autosomal dominant PKD
colon covered in ademotous polyps after puberty
familial adenomatous polyposis
inhertited disorder of blood vessels with branching skin lesions, epistaxis, skin sidocoloration, AV malformations, GI bleeding, hematuria
hereditary hemorrhagic telangactasia
spheroid RBC and defect in spectrin and ankyrin. increased MCHC and increased RDW and treated with splenectomy
hereditary spherocytosis
dpression, and progressive dementia, choreiform movements, caudate atrophy- increased dopamine, decreased GABA, increased ACH in the brain- what chromosome and defect
Huntington and chromosome 4
abnormaility which leads to multiple malignancies at a young age- have sarcoma, breast, leukemia, and adrenal gland cancer, osteosarcoma, and brad adenocarcinoma what is mutated
Li Fraumeni- p53
what is the defect in the gene causing talk, long extremities, precuts excavate, hyperbole joints, and long fingers and toes, and cystic medial necrosis of the aorta, and floppy mitral valve with aibluxation of the lens upward
marfan defect in FBN1 and chromosome 15 fibrillin defect
osteomas, lipomas, sebaceous cysts, and colon polyps and cancer
Gardner syndrome
what genetic condition have the increased risk of rhabdomyosarcoma of the heart
Tuberous scleorsis
what disorder is characterized by RCC pro, angiogenic growth factors, and hemangioblastomas- what chromosome and what defect
VHL and its chromosome 3 tumor suppressor
what does dystrophin do and what is the mutation that covers duchenne
link actin to transmembrane proteins- frameshift
what is the mutation for becker that causes it
non-frameshift- truncated but somewhat functional gene
muscle wasting, catarats, testicular atriphy and frontal balding, arrhythmia- what causes it
CTG repeasts in the DMPK gene that causes abnormal expression of myotonin protein kinase-
large testicles, mental retard, long face, large jaw, everted ears, autism, mitral valve prolapse- what gene and inheritance pattern
Fragil X mutation in the FMR1 gene with trinucleotide expansion
what is the translocation that can cause Downs syndrome
14;21
severe intellecutal disability, rocker bottom feet, microagnathia, low set ears, clenched hands, overlapping fingers, congenital heart disease- whats on the quad screen and disease
trisomy 18 and decreased everything
severe intellectual disability, rocker bottom feet, microphthalamia, microcephaly, cleft lip and palate, holoprosenscepahly, polydactyl and congentiac heart disease and cutis aplasia- quad screen and disorder
trisomy 13 and decreased hcg
woman has multiple miscarriages but when she has the a child, it has dismorphic features and lots of organ abnormalities
unbalanced robertsonian translocation
microcephaly, moderate intellecutal disability, high pitched cry, epicentral folds, and cardiac abnormalities- what is it called and why does it happen
cri du chat syndrome- microdeletion on chromosome 5
elf face, disability, hypercalcemia, and well developed verbal skills, friendly and cardiac problems- what is the disorder and genetics
Willimas and micro deletion on chromosome 7
hypocalcemia, T cell deficiencyy, and cardiac defects like tet of fallot and truncus- what is the defect and gene
22q11 and Digeorge syndrome- no 3 and 4th branchial pouches
what are the fat soluble vitamins
A, D, E, K
what vitamins can be produced by enteric bacteria
folate and vitamin K
what is the vitamin profile after gastric bypass
increased K and folate from bacterial overgrowth and decreased B12, A, D, E, iron
deficiency of this causes night blindness, dry scaly skin, corneal degeneration, some immunosuppression
vitamin A
excess from acute toxicity leads to nausea vomitting vertigo, and blurred vision
vitamin A
chronic toxicity leads to apologia, dry skin, arthralgia, and pseudo tumor cerebri
vitamin A
what can vitamin A be used to treat
AML M3 subtype and measles
deficiency of this: ATP depletion, worked by glucose infusion, highly aerobic tissues are hit first.Start to see with alcohol chronically. Confusion, opthmalplegia, personality change, ataxia, confabulation, personality change, an memory loss. damage to medial dorsal nun the thalamus and maxillary bodies. dry beriberi- polyneuritis and symmetrical muscle wasting. wet is high output cardaic failure and edema
thiamine defiency loss of pyruvate dehydrogenase,e alpha ketoglutartate, transkelotase, and branched cain amino acids
what is the first enzyme in alcohol metabolism
alcohol dehydrogenase
what drug blocks the first step of alcohol metabolism and what is the use for it
fomepizole- it is used an the antidote for methanol and ethylene glycol toxicity
what is the second enzyme in the alcohol metabolism pathway
acetaldehyde dehydrogenase
what blocks the second step of alcohol metabolism
disulfiram
why does alcohol causes steatosis
it increases the NAD/NADH ratio so that it is metabolized instead of close and it used the malate shunt instead so that it prevents gluconeogenesis as well
In what organelle has fatty acid oxidation, acetyl coA production, TCA, oxidative phosphorylation, ketogenesis
mitochondria
where in the cell has glycolysis, HMP shunt, and synthesis of steroids, proteins, and carry acids, nucelotides
cytoplasm
autosomal recessive defect in an enzyme leads to increased methylmalonic acid so metabolic acidosis, hypoglycemia from increased basal metabolic rate leads to increased ketones which leads to AGMA. This inhibits the urea cycle which leads to hyperammonia- hypotonic, lethargic, vomitting, respiratory distress- increased urine propionic acid and methylamalonic acid- what enzyme is deficient
methylmalonic acid mutatse
what is the GLUT for hepatocytes and Beta cells of the pancreas
2
what is the GLUT for neurons and placenta
3
what is the GLUT for fructose in the GI tract
5
what is the GLUT for RBC, BBB, and is generally independent
1
what is the GLUT for skeletal muscle and adipose which is insulin dependent
4
what is the first enzyme in the glycolytic pathway
hexokinase and glucokinase
what is the rate limiting enzyme of glycolysis and what regulates it
PFK 1- increased AMP and fructose 2,6
what down regulates the rate limiting step of glycolysis
increased ATP and citrate from the TCA cyle
what enzyme takes phosphoenolpyruvate to pyruvate
pyruvate kinase
what is pryruvate kinase stimulated by
fructose 1,6 bisphosphate
what down regulated pyruvate kinase
ATP and alanine
what is the deficiency if there is hemolytic anemia due to inability to maintain Na-K ATPase
pyruvate kinase deficiency because the RBC can only go through glycolysis to produce ATP
in the well fed state, which enzyme is stimulated in the fructose 6-P pathway
PFK2 is stimulated so that fructose 2,6 bisphos is increased which turns off glycolysis and k creased glycolysis
in the fasting state, which enzyme is stimulated in the fructose 6p pathway
FBPase is stimulated so fructose 2-6 goes to frucuctose 6p and gluconeogenesis
what are the fates of pyruvate
odd chain FA propyl coA, TCA as oxaloactetate, and AA as oxaloacetate
what is the rate limiting step of gluconeogenesis
fructose 1,6 bisphosphatase
what increases and decreases the rate limiting enzyme of gluconeogenesis
ATP increases it and AMP decreases it
neurologic defects, lactic acidosis, increased alanine and can be from B1 deficiency or arsenic exposure-
pyruvate dehydrogenase complex deficiency- a buildup of pyruvate gets shunted to lactase and alanine- treatment is a ketogenic diet like lysine and leucine
pyruvate to alanine aminotransferase requires what cofactor
b6
pyruvate to oxaloacetate for the TCA cycle of gluconeogenesis requires what cofactor
biotin- pyruvate decarboxylase
pyruvate to glycolysis to TCA by pyruvate dehydrogenase requires what cofactors
B1, B2m B3, B5
pyruvate to the lactic acid cycle is major pathway in what tissues and requires what
RBC, WBC, kidney medulla, lens, testes, and cornea- B3
What is the first enzyme in the TCA cycle
citrate synthase take acetyl cos and oxaloacetate to citrate
what is the rate limiting enzyme of the TCA cycle
isocitrate dehydrogenase
what is the most heavily regulated step of the TCA cycle and what regulates it
alpha ketoglutarate dehydrogenase- requires B1, lipoic acid, B5 ,B2, B3- yields 1 GTP, 3 NADH, and FADH2
what inhibits complex 1 of the OxPhos
amytal and rotenone and BMDP
what inhibits complex 3 of OxPhos
antimycin
what are rotenone and antimycin
fish poisons
what inhibits complex IV
cyanide, sodium azide, CO, and hydrogen sulfide
what inhibits ATPase of ox phos
oligomycin A- macrolide
what are the uncoupling agents of oxphos
high dose aspirin and 2,4 DNP
what does the HMP shunt do
its provides NADPH from glucose 6P which is required for reduction reactions and it veils ribose for nucleotide synthesis and glycolytic intermediates
what is the rate limiting step in oxidative HMP shunt
glucose 6p dehydrogenase
what is the rate limiting step in the non oxidative HMP shunt and what does it require
B1 and it is phosphopentose isomerase or transkelotases
Patient has hemolytic anemia following sulfonamide treatment- what does the patient have, what else can set it off, and why does it happen
It is G6PD deficiency. NADPH is necessary to keep glutathione reduces which detoxifies free radicals and peroxides. The decrease in NADPH production in RBC leads to hemolytic anemia due to poor RBC defense against oxidizing agents. Infection can precipitate hemolysis and inflammatory response produces free radicals that diffuse into the RBC causing the damage. Drugs: fav beans, sulfonamides, primaquine, anti-TB drugs- confers malaria resistance
what cells are seen with G6PD deficiency
heinz bodies- denature hemoglobin precipitates in the RBC due to oxidative stress, and bite cells which are the result of phagocytic removal of the Heinz bodies by splenic macrophages
what enzyme in the HMP shunt pathway neutralizes the H2o2
glutathione peroxidase
patient presents with fructose in the blood and urine- what is the deficient enzyme, condition, and inheritance
essential fructosuria, def in fructokinase, AR
patient has hypoglycemia, jaundice, cirrhosis, and vomiting after consumption of fruit, juice, and honey in a smoothie- what is the deficient enzyme, what is the condition, what is the treatment
fructose intolerance, deficiency in aldolase B, AR, fructose 1P accumulates, whcich decreases the available phosphate which causes the symptoms because it blocks glycogenolysis and gluconeogenesis. Urine dipstick will be negatie. Decrease the consumption of fructose and sucrose
patient has galactose in the blood and urine following feeding and has infantile catcalls and cannot track objects and does not have a social smile. what is the deficient enzyme, what is the condition, what is the treatment
Galactokinase deficiency- galactokinase- galactitole accumlates and it is AR. It appears when they start feeding- tends to be mild treat with reduced galactose in the diet
patient has failure to thrive, jaundice, hepatomegaly, infantile cataracts, intellectual disability and has had neonatal ecoli sepsis- what is the deficient enzyme, what is the condition, what is the treatment
classic galactosemia- absence of galactose 1 P uridyltransferase AR- damage is accumulation of galactitol in the lends and other ares of the body need to exclude galactose and lactose in the diet of the newborn
what enzyme converts glucose to sorbitol and sorbitol to fructose
aldose reductase and sorbitol dehydrogenase
what cells/tissues can do the full conversion of glucose to fructose
liver, ovaires, and seminal vesicel
what cells/tissues only have alludes reductase
schwann cells, retina, kidneys
what happens to sorbitol conversion in a hyperglycenic state
aldose reductase converts glucose to sorbitol faster than it can be metabolized and this lets increased sorbitol accumulate and increased water can diffuse into the cells. The NADPH is depleted which increases oxidative stress which accelerates the development of cataracts and diabetic microvascular complications
patient has bloating, cramps, flatulence, and osmotic diarrhea what is the deficient enzyme, what is the condition, what is the treatment
lactase deficiency- stool has decreased pH and increased hydrogen content and there is normal mucosa there is osmotic diarrhea due to the extra stuff in the lumen of the gut
what are the essential amino acids
methionine, valine, histidine, isoleucine, phenylalanine, threonine, tryptophan, leucine, lysine
what are the acidic amino acids
aspartic acid and glutamic acid which are negatively charged at body pH
what are the basic amino acids
arginine and lysine and histidine
what enzyme takes CO2 and Nh3 to carbamoyl phosphate
CPS1
what enzyme takes ornithine to citruline with carbamoyl phosphate
ornithine transcarbamylase
explain alanine role in transport of ammonia
alanine is release by muscle during protein catabolism as part of the glucose alanine cycles that removes excess nitrogen. Alanine goes to the over as a vehicle of nitrogen disposal and it is then used as a carbon source for gluconeogenesis. Alanine is transaminated to form pyruvate and alpha ketoglutarate which accepts the amino group. Glutamate then receives the amino group and releases ammonia to regenerate the alpha ketoglutarate
patient has tremor, slurring of speech, somnolence, vomiting, cerebral edema, and blurring of vision from accumulation of this why does it happen
excess amminoia depletes the alpha ketoglutarate and this leads to an inhibition of the TCA cycle
treatments for hyperammonia
lactulose which acidifies the GI tract and traps the ammonium, rifaximin to decrease colonic amminogenic bacteria, benzoate, phenyl acetate, and phenylbutarate bind to NH4 and lead to increased excretion of it
neonate with poorly regulated respiration and body temperature, poor feeding, developmental delay and intellectual disability-what is the deficient enzyme, what is the condition, what is the treatment
absence of N acetyl glutamate which is a required cofactor for CPS1
patient has increased orotic acid in the blood and urine and decreased BUM, hyperammonenmia, and no megaloblastic anemia- vomitting confusion, coma, tachypnea-what is the deficient enzyme, what is the condition, what is the treatment
Ornithine transcarbamoylase deficiency which is X linked recessive- it interfers with ability to eliminate ammonia.
child has vomiting, poor feeding, and urine smells like burnt sugar, CNS defects, and intellectual disability- what is the deficient enzyme, what is the condition, what is the treatment
MSUD- blocked degradation of branched chain amino acids like isoleucine, leucine, and valine due to decreased branched chain alpha ketoacid dehydrogenase cases increased lupine. Need to restrict the ILV and supplement with thiamine
blue-black connective tissue and sclerae, urine turns black with prolonged exposure to air and has arthritis-what is the deficient enzyme, what is the condition, what is the treatment
homogentisate oxidase in the tyrosine degradation pathway of tyrosine to fumarate. It is benign but the homogentisic acid is toxic to cartilage
patient has increased homocysteine in the urine, intellectual disability, marinades, osteoporosis, lens subluxation down and in and thrombosis and atherosclerosis-what is the deficient enzyme, what is the condition, what is the treatment
can be from cystathione synthase deficiency which can be treated with increased cysteine and B12 and folate. or from decreased affinity of cystathione synthase for pyridoxal phosphate- treat with increased B6 and cysteine. Methionine syntheses def- decrease methionine in the diet and try B6
patient has recurrent hexagonal stones in the urethra-what is the deficient enzyme, what is the condition, what is the treatment
defect of renal PCT and intestinal amino acid transporter that prevents reabsorption of cysteine, ornithine, lysine, and arginine- the excess cysteine forms these stones. Treat with urinary alkalization or good hydration
what is the type of bond are the branches of glycogen
alpha 1-6
what is the type of bond that holds together the glycogen linkages
alpha 1-4
what are the tone bodies
acetone, acetoacetate, and beta hydropxybutyrate
refeeding syndrome
negligible nutrient intake for five days to intracellular stores depleted. Body takes all of the new nutrients into the cells which decreased the blood levels which can depletes ATP from trapping nutrients in the cells
starvation at 1-3 days- what maintains everything
hepatic gluconeogenesis, adipose release of FFA, muscle and liver shift to FFA, hepatic glucose from lactase and alanine and from adipose tissue odd chain fatty acids
when are glycogen stores depleted
1 day
starvation what maintains everything
adipose stores which are being used by the brain as ketones. after this is depleted, protein degradation accelerates leading to organ failure. Amount of excess stores determines survivial
apoE
mediates remnant uptake
apoA1
activates LCAT
apoC2
lipoprotein lipase cofactor
apoB48
mediates chylomicron secretion
apoB100
binds LDL receptor
LDL transports cholesterol to
the tissue from the liver
HDL transports cholesterol to
the liver from the tissue
chylomicro
delivers diet TG to tissue and delivers cholesterol to the liver in the form of remnants
VLDL
delivers hepatic TG frto perioheral tissue
IDK
formed in the degradation of VLDL and delivers TGS and cholesterol to the liver
LDL
delivers heaptic cholestorl to the peripheral tissues
HDL
mediates reverse cholesterol transport and are increased in alcohol synthesis
capsule
prevents phagocytosis
glcocalyx
mediates adherence to surfaces and can form the biofilm
periplasm
the space between the cytoplasmic membrane and outer membrane of gram negative bacteria with the peptidoglycan wall in the middle
outer membrane
contains the LPS which is the endotoxin for TNF alpha and IL1
lipotechoic acid
extend from the membrane to the outside and this acts as the inducer of TNF and IL1 in gram positive infections
where are the beta lactamases located
in the periplasmic spaces
which bacteria are filamentous and what are their oxygen requirements
nocardia(aerobe) and actinomyces(anaerobe)
which bacteria have no cell wall
mycoplasma, ureaplasma
which bacteria are spirochetes
borrelia, leptospira, and treponema
bacteria that does not gram stain well
treponema, leptospira, mycobacteria, mycoplasma, ureaplasma, legionella, rickettsia, chlamydia, bartonella, ehrlichia, anaplasma
what does PAS stain diagnose?
whipple disease- trophema whippeli
which bugs are intracellular
legionella, rickettsia, chylamydia, bartonella, ehrlichia, anaplasma
Ziehl Neelsen stain- carbol fuchin
acid fast bacteria
india ink stain
cryptococcus neoformans
silver stain
fungi and legionella, helicobacter pylori
what is the difference between selective and differential media
selective- factors particular organism and indicator has a color change with certain bacteria but does not inhibit growth of others
Thayer Martin media
selective for Neisseria by inhibiting the growth of other organisms with the antibiotics
tellurite agar
diptheria- growths with black iridescent colonies
pink colonies on MacConkey
lactose fermenters
anaerobic bacteria
clostridium, bacteriodes, fusobacterium, actinomyces
obligate intracellular bactera
rickettsia, chlamydia, coxiella- rely on host ATP
facultative intracellular bacteria
salmonella, neusseria, brucella, mycobacteria, listeria, francisella, legionella, yersinia pestis
encapsulated bacteria
pseudomonas, strep pneumo, haemophilus, flu b, neisseria meningitis, ecoli, slamonella, klebsiella, group B strep
what patient population has an increased risk of infection from encapsulated bacteria
asplenic patients
which are capsular vaccines
s pneumo, h flu, and meningitis
organisms that cause stag horn calculi and why
creases positive- proteus, ureaplasma, staph saptophyticus
catalase positive and what disorder has increased risk of these infections
nocardia, pseudomonas, listeria, aspergillus, candida, ecoli, staphylococci, serratia, b.cepacia, h pylori
yellow sulfur granules
actinomyces
blue green pigment
pseudomonas
yellow pigment
staph arueas
red pigment
serratia
biofilm on catheter and prosthetic valves
staph epi
biofilm on dental plaques and infective endocarditis
viridans strep
biofilm in CF patients in lung and contact lens ketatosis
pseudomonas
protein A
binds the Fc region of the IgG to prevent opsonization and phagocytosis- s aureus
enzyme that cleaves IgA
s pneumo, hib, neisseria and use to it adhere to the mucosa
helps prevent phagocytosis
group A strep and causes the long term issues with strep
ability to take up naked DNA from the environment and what bacteria can do this
its called transformation and it is done my strep pneuma and hi and neusseria- if deoxyribonuclease is added the environment then it can not longer transform it
transfer of plasmid from one bacteria to another
conjugation
segment of DNA that can jump from one location to another and can transfer genes from plasmid to chromosome and vice versa. When excision occurs it can include some flanking chromosomal DNA which can be incorporated into a plasmid and transferred to another bacteria
transposition
lytic phage infects bacteria leading to cleavage of bacterial DNA. Parts of bacterial chromosomal DNA may be in the phage capsid. Phage infects another bacteria which transfers these genes
transduction
lysogenic phage infectes bacteria and viral DNA is incorporated into the DNA and its in the phage capsid for another bacteria- what bacteria toxins are in lysogenic phages
specialized transduction- botulinum, group a strep, cholera, diphtheria, shiga toxin
what kills spores and how long
autoclave with steam at 121 for 15 minutes
what produces spores
bacillus, clostridium, and coxiella
what is an endotoxin
Lipid A from LPS and it has shock, fever, hypotension, DIC, from induction of TNF, IL1, and 6
what is an exotoxin
it is a polypeptide and it is a low infective dose
alpha hemolytic bacteria
strep penumo and viridans strep
beta hemolytic bacteria
s bureaus from secretion of hemolysin and strep progenies and strep agalactiae
gram positive beta hemolytic catalase + coag+ clusters
staph aureus.
short incubation of food poisoning- vomitting
s aureus food poisoning
fever rash, vomiting, desqamation and shock with end organ failure associated with tamposn
s aureus TCC it binds the MHC II and TCR to induces this damage
normal flora that is gram + catalase + and coagulase - urease - in clusters that are novobiocin sensitive- it an cause infection of prostethic devices and IV catheters
staph epi
gram + coag- cata + cocci urease +novobiocin resistant- normal flora of perineum
staph saprophyticus
gram positive lancet shaped diplococci, encapsulated that is optician sensitive causes meningitis, otitis media, pneumonia sinusitis, rusty sputum- can undergo natural transformation
strep pneumo
what patients are at an increased risk of sepsis from strep pneumo
sickle cell and asplenic
gram positive alpha hemolytic cocci that are normal in the oropharynx and can cause dental caries- this can cause subacute bacterial endocarditis- optician resistant
strep viridans- they are not afraid of the chin (optochin) because they live in the mouth
gram positive cooci pyogenic infection causing pharnygitis, cellulitis, impetigo, and erysipalas
strep pygenes
gram positive cocci- scarlet fever tS, necrotizing facitis
strep pyogenes
criteria or acute rheumatic fever
polyarthritis, carditits, nodules, eryhtema marginatum(central clearing), chorea
blanching, sandpaper body rash, strawberry tongue, and circumpolar pallor after strep A pharyngitis
scarlet fever
gram positive, colonized vagina and causes meningitis, spots, and pneumonia in babies- produces a factor that increases hemolysis
strep B
when do you screen moms for strep B
35-37 weeks
gram positive cocci causing subacute endocarditis- what cancer and what bug
strep bovis- colon cancer
gram positive cocci- normal colonic flora that are resistant to pcn and can cause UTI biliary tract infections, and subacute endocarditis following GI or GU procedures
enterococci
what is enterococcus often resistant to
vancomycin
only bacteria with polypeptide capsule- that contains d-glutamate
bacillus anthracis
painless papule surrrounded with vesicle with a painless necrotic eschar that can progress to bacteremia
b.anthracis
inhales spores leads to flue symptoms and rapidly progressing fever, pul hemorrhage, and medisatinitis and shock after exposure to wool
b. anthracis
reheated rice food poisoning with vominting after 1-5 hours with preformed txon
b. cererus
produces after a penetrating would with contractors from the blockade of inhibitory NT spastic paralysis- how to treat and what causes
c. tetani- antitoxin and vaccine booster and diazepam and debride- can be from umbilicus in newborns
heat labile toxin inhibtis ACH release at the NMJ- ccuases flaccid paralysis- what is different with babies who have get this- what is the exposure
it is c botulinum and babies get it from ingesting the spores in honey which leads to the disease and these germinate in the GI tract. Adults ingest it from home-canned food and its a preformed toxin
produces alpha toxin causing myonecorsis and hemolysis- it has gangrene with are lesions
c perfringens- anaerobe
spores can survive in undercooked food and are a heat labile enterotoxin- from the same thing that causes gas gangrene
c perfringens
pseudomembranous colitis with a toxin A that binds the brush border of the gut and a toxin B that causes cytoskeletal disruption via actin depolymerization and diarrhea- usually with antibiotic like cloned or ampicillin use
c diff
gram positive rods, beta prophage withe the toxin and it inhibits EF2. it causes pseudomembranous pharyngitis with lymphadenopathy, myocarditis, and arrhythmias-
cornybacterium dipteheria
gram positive facultative intracellular rod- from dairy products, cold cut meats, and transplacental or from birth canal- have rocket ails that allow intraceullar movement and tumbling motion in the broth- can cause amnionits sepsis and spontaneous abortin in pregnancy, neonatal meningtitis, gastroenteritis in adults
listeria
acid fast aerobic, filamentous with pulmonary infections in the compromised and cutaneous infections in immunocompotent
nocardia
non acid fast, anaerobe with norm oral, GI, and reproductive flora- causes oral and facial abscess with draining sinus tract and self granules and can be from PID with IUD
actinomyces
lower lobe with ipsilateral calcified ln with TH1 mediated caveating necrosis with a ghon complex with the hilar nodes
primary TB
fibrocaseous cavitary lesion in the apex with liquefactive necrosis and erased the pulmonary vessels occasionally leading to hemoptosys and persistent cavitation can lead to aspergillus
reactivation of TB
milliary TB
spread to meinges, vertebrae, lungs, LN, spleen, bone,s adrenals
vertebral TB disease
Potts disease
AIDs Tb with resistance to multiple drugs
MAC- use prophylactic azithromycin
mycobacterium marnium
infection on aquarium handlers
night sweeats, fever, weight loss, cough, hemoptysis
tb
what is cord factor in TB
it is a serene cord appearance that inhibits macrophage maturation and induces the release of TNF alpha- which then increases the virulence
diffuse skin involvement with lion face and is high TH2 response with communicable- tends to be in compromised patients
lepromatous
hairless plaques, and these lesions have no feeling in them- cell mediated immunity is mainly a TH1 response
tuberculoid leprosy
what bacteria ferment lactose
klebsiella, ecoli, enterobacter, and serratia
reinfection with an STD because of
antigenic variation of the pilus on neusseria gonocci
septic arthritis, neonatal conjunctivitis, PID and fitzhugh curtis syndrome with gram negative diplococci that are often intracellular- there is sexual transmission and can cause blindness in newborns
n gonnorhea
gram negative diplococci that causes meningitis and has a capsule the B type capsule is most common- can have petechial hemorrhages, gangrene of the toes, and waterhouse freidericheson wit hDIC
causes my n meningitis
neisseria infections are increased in which deficiency
people who don’t form membrane attack complexes
small gram neg coccobaccilus with aerosol transmission- nontypable cause miucosal infections like otitis media, conjunctivitis and bornchitis
non-encapsulated homophiles influenzae
the encapsulated strain causes epiglottis which has stridor and drooling, meningtitis, pneumonia and otitis medai
capsulated HIB
what is the prophylaxis for close contacts to HIB
rifampin
gram negative aerobic coccobacillus that and cause tracheal cytotizin and a paradoxical cough and it has a long cough term
bordatella pertusis
gram negative rod that can be seen with silver stain, grows on charcoal with iron an cysteine with aerosol transmission from environmental water source causes severe knomonia that is unilateral and lobar-
legionella
mild flu like illness from gram negative rod that can be seen with silver stain, grows on charcoal with iron an cysteine with aerosol transmission from environmental water source causes severe
pontiac fever with legionaires
aerobic motile gram negative rod that can ferment oxidase and produces pyocyanin and endotoxin, exotoxin that inactivates EF2 and phospholipase C- pneumonia, sepsis, erythema gangrenosum (necrotic skin ulcers), indwelling catheter associated UTi, and otitis extern, nosocomial infections, hot tub folliculitis
pseudomonas
colonizes lung of CF patients and has mucoid capsule
pseudomonas
treatments for pseudomonas
carbapenems, aminoglycosides, monobactams, polymyxins, FQs, 3-4 generation cephalosporins, piperacillin, ticaricillin.
microbe invades the intestinal mucosa causing necrosis and inflammation- which ecoli
EIEC like shigella
produces heat labile and stable enterotoxin but no inflammation or invasion- diarrhea from mexico
travelers diarrhea- ETEC
no toxin produced adheres to the apical surface and flattens villi and prevents absorption- diarrhea in children
EPEC-
undercooked beef or raw veggies- anemia, thrombocytopenia, and acute renal failure due to micro thrombi forming on damaged endothelium and causes mechanical hemolysis with schistocytes on the peripheral blood smear-platelets are consumed and decreased renal blood flow occurs
EHEC- shiga toxin
gram negative rose that causes lobar pneumonia from aspiration with mucoid colonies from polysaccharide capsules and has currant jelly sputum- can also cause liver and lung abscesses tends to occur in alcoholics or diabetics
klebsiella
gram negative comma or s shaped bacteria with polar flaglaa that is oxidase positive- it is bloody diarrhea in child with fecal oral transmission that can come from infected animals like puppy with diarrhea
campylobacter jejuni
what can campylobacter jejune cause
GB or reactive arthtisis
bacteria with swarm mobility and is urease positive that form stag horn calculi
proteus
need a high dose to get inoculated because gastric acid can neutralize it, antibiotics prolong the excretion- can cause rose spots on the abdomen, constipation, and absomial pain with ever- has capsule that can prevent opsonization- can hide in the gall bladder for carrier state colonization
salmonella typhi
anibiotics prolong duration and have bloody diarrhea from poultry, eggs, pets, and turles- gastroenteritis
all other salmonella
what can cause osteomyelitis in sickle cell patients
salmonella
bloody diarrhea with invasion of the organism during invasion
shigella
gram negative flagellated comma shaped oxidase positive profuse watery stool with increase cMP and Gs from the enterotoxin requires a large inculum unless there is a decrease in gastric acid
vibrio cholerae
gram negative rod that is transmitter by pet feces like puppies or milk or pork can cause acute diarrhea or pseudoappendicitis
yersinia enteroclitica
curved rod with terminal flagella gram negative- catalase, oxidase and urease positive. colonizes the antrum of the stomach, gastritis and peptic ulcers and increased risk of peptic ulcer disease, gastric adenocarcinoma and MALT lymphoma
hpylori
treatment for hpylori
amoxicillin, clarithromycin, PPI
spirochete found in water with animal urineflu with myalgia of the calves, jaundice, and photophobia typically seen in surfers in the tripics
leptospira interrogans
sever jaundice and azotemia from liver and kidney dysfunction with fever, hemorrhage and anemia
Weil disease- leptospira interrogate
what is lyme disease transmitted by
ioxedes tick
what is stage 1 of lyme
erythema migrants and flu
second stage of lyme
secondary lesion, pancarditis, AV block, facial nerve palsy, migratory myalgias and transient arthritis
third stage of lime
encephalopathies and chronic arthritis
primary syphilis
painless chancre and can see organism on darkfield
secondary syphilis
maculopapular rash on palms and sles, condyloma lata, lymphadenopathy, patyhc hair loss
tertiary syphilis
gumbos with parotitis with vasa vasorum destruction and neurosyphilis from loss of doral columns, argyll robertson pupil- accomidae but won’t react.
congenital syphilis
facial abnormality and snuggles, saddle node, hotchinsom teath, saber shints, mulberry molars, and VIII deafness
false postives on the VDRL lab
viral infection, drugs, rheumatic fever, lupus, leprosy
what can happen after treating syphillis
can feel like the flue from the destruction of the spirochetes
what transmits anaplasmossi
ixodes
what transmits bartonella
cat scratch
what transmits barely burgorderi
ixodes tick
what transmits borrelia recurrentis
louse
what transmits brucella
unpasteurized dairy
what transmits campulocbater
pets and people
what transmits chlamyydphila psittaci
parrot
what transmits coxiella burnetii
aersol of cattle and sheep
what transmits ehrlichia
ambyloma
what transmits francilla
rabbit
what transmits leptospirsa
animal urine
what transmits pasturella
animal bite
what transmits rickettsia prowazekii
human to human or louse
what transmits rickettsia ricketsii
dog tick
what transmits rickettsia typhi
fleas
what transmits salmonella
reptiles and poultry
what transmits yersinia pestis
flea and prarie dogs
pleomorphic gray vaginal discharge with fishy smell clue cells with stippled appearance
gardnerella
disease occurs in south atlantic states like north carolina with rash that starts at wrists and ankles and moves to the trunk and palms and soles- headache, fever, rash
rickettsi rickettsii
fleas causing rash that starts centrally and spreads out can also be from the louse
rickettsii type and prowazeki
monocytes with mulberry inclusions tick vector
ehrlichiosis
tick vector with granulocytes and morula
anaplasma
spores inhaled by aerosol and causes pneumonia and culture negative enodcarditis- typically intracellular and from cow placenta
coxiella burnetti
choinc infection causing blindness from follicular conjunctivitis in africa
chlamydia A,BC
urethritis and PID, ectopic preg, neonatal pneumonia with staccato cough, and eosinophilia, neonatal conjunctivitis
DK clap
small painless ulcers on the genitalia with swollen inguinal lymph nodes that ulcerate into buboes
L1,L2,L3 clap
intracellualr infection with elementary bodies that enter the cell via endocytosis and go to the reticulocytes body which replicates then reorganizes to travel
chlamydia
can case follicular conjunctivitis, nongonococcal urethrtitis and PID, prostatitis
chlamydia
what fungus type grows at cold temperature
mold
what fungus type grows at hot temperatures
yeast
dimoprhic fungus from bat and bird droppings from macrophages filled with RBC and ovoid cells within the macrophages
histoplasmosis
dimorophic fungus from the US and central america- inflammatory lung disease and can disseminate to skin and bones, and forms granulomatous nodules. It is broad based budding yeast- thick wall round yeast with broad based buds
blastomycosis
SW Us and California, and causes pneumonia and meningitis and can disseminate to the skin and bone can increase rate after earthquakes. Can get some arthritis and skin findings. Spherule filled with endospores
cocciodomycosis
budding yeast with captains wheel formation much larger than RBC- severe pneumonia with granulomas
paracoccidiomycosis
what are the types of tinea
microsporidium, trichophytan, and epidermophyten
what is fungal on the head called
tinea capitus
what is dermatophye on the body called and looks like ring worm
tine coporis
what is dermatophyte on the feet called
tinea pedis
what is dermatophyte on the nail called
tinea unguium
spagetti and meat balls appearance on the slide and hypo pigmented lesions with degradation of lipids that produces acids that damage the melanocytes in those areas
tina versicolor or pitaryasis or malassezia furfur
dimorphic fungus with psudeohyphae and budding yeasts and germ tubes. These can cause a superficial infection (neutrophils are used for it) and systemic is mediated by T cells not working. Esophageal thrush is in immune compromised and vulvocaginitis, diaper rash, endocarditis of drug users, and can be chronic in SCIDs
candida albicans
what is the treatment for Candida
topical azole, nystatin, or ampho B if systemic
septate hyphae at 45 degree angles- produce conidia and can cause lung infection on preexisting evacuations from TB.
aspergillus
aspergillus can have reaction in what other condition
asthma
what kind of cancer comes from afalatoxin
hepatocellular carcinoma
narrow budding heavily encapsulated yeast found in pigeon droppings, and inhalation with hematogenous dissemination to meninges. Latex agglutination detects capsular antigen. Can start as symptomatic lung infection then meningoencepahlitis and then it is budding year with a thick capsule
cyptococcus
what do the brain lesions look like in cyptococcus meningoencephalitis
soap bubble lesions
what type of patients are more susceptible to moocher and rhizopus
DKA and neutropenic patients (leukemia)
irregular broad non spectate hyphae at wide angles and they proliferate through blood vessel walls causing them to penetrate the cribriform plate and enter the brain. Rhino cerebral frontal lobe abscess and cavernous sinus thrombosis- headache, facial pain, black necrotic eschar on face with cranial nerve involvement
Mucor and Rhizopus
diffuse intersitial pneumonia with yeast like fungus that is inhaled. Most are asymptomatic unless they are compromised with AIDS. Bilateral ground glad opacities on CXR.
PJP
what is the prophylaxis for PJP and when to start
TMP-SMX and its when CD4 drops below 200
dimorpic cigar shaped yeast that grows in branching hypes with rosettes of conidia. Lives on vegetation it is usually from thorn and it cause local pustule or ulcer with nodules along draining lymphatics
sporothrix schenckii
what is the treatment for sporothrix
potassium iodine and itraconazole
bloating flatulence, foul smelling diarrhea and seen in campers- transmission, protozoa, and treatment
giardia, from cysts in the water, pear shaped ova, have four flagella, and can do metronidazole
bloody diarrhea, liver abscess with anchovy paste, RUQ and flask shaped ulcer- transmission, protozoa, and treatment
cysts in the water fecal oral, entamoeba histolytic, and metronidazole and iodoquinol
severs diarrhea in AIDs patiens mild disease in noncompromised- transmission, protozoa, and treatment
oocysts in water, fecal oral or person to person, and acid fast pink oocytes on the stain- cryptosporidium- can be treated by filtering the water supply or nitazoxanide
congenital infection with choreoretinitis , hydrocephalus, and intracranial calcifications- transmission, protozoa, and treatment
toxoplasmosis, cysts in meat or cat feces, and sulfadiazine and pyrametahmine
AIDS has a brain abscess that is seen as a ring enhancing lesion- transmission, protozoa, and treatment
cysts in meat or cat feces, toxoplasmosis, and sulfasizine and pyrimethamine
enlarge LN, recurring fever, somnolence and coma- transmission, protozoa, and treatment
tsetse fly, and trypanosome brucei, and trypomastigote in blood smear that looks like a ribbon- suramin
what do the fevers with trypanosome go up and down
antigenic variation
what plasmodium has a 48hour cycle
vivax and ovale
what plasmodium has a 72 hour cycle
malariae
what is the transmitter of malaria
anopheles mosquito
which malaria is the more virulent strain
falciparum
what kinds do you use primaquine for
vivax and ovale
what do you see on blood smear
trophozoite ring in the RBC
fever, hemolytic anemia, northeastern US and increased risk in asplenic- transmission, protozoa, and treatment
ixodes tick can have lyme disease too, maltese cross and rinks in the TBC, and treat with atovaquine and azithromycin
dilated cardiomyopathy with apical atrophy, megacolon, megaesophagus, from south america, and unilateral swelling of the orbiatal characteristic of the acute stage. transmission, protozoa, and treatment
reduviid bughas feces deposited into the bite- trypomatigote in the blood smear- bennidazole and nifurtimox- chagas disease in trypanosoma cruzi
spiking fevers, hepatosplenomegaly, pancytopenia, and can be big skin ulcers if only cutaneous- transmission, protozoa, and treatment
sandfly- leishmania donovani- macrophages contrain amistigotes- ampho B
foul smelling green discharge itching burning- sexual contact see trophozoites and a strawberry cervix- transmission, protozoa, and treatment
trichomonas vaginalis- treat with metronidazole
which nematodes are ingested
enterobius, ascaris, toxocara, trichinella
what nematodes are cutaneous
strongyloides, ancylostoma, necator
what nematodes are from bites
loa loa and onchocerca volvulus, and wuchereria bancrofti
what is the immune response to helminths
eosinophils are acted on by type I and II HSN reactions and these are in response to helminths. Type I neutralization of histamine and leukotrienes. Type II is eosinophils attach to surface of helminths via IgE and release cytokines contain in the granules. Eosinophils are secreted by Th2 secreting IL5 for the binding of IgE to the Fc portion it then degranulates leading to MBP being released and antibody dependent cell mediated cytotoxic killing
intestinal infection causing anal pruritis- transmission, helminth, and treatment
scotch tape test, decal oral- enterobeus vermicularis, bendazoles
intestinal infection with possible obstruction of the ileocecal valve- transmission, helminth, and treatment
ascaris lumbricoides- fecal oral visible feces under microscope, bendazoles
intestinal infection cauing anemia by sucking blood from intestinal wall can have puritic serpiginous rash from walking on the beach barefoot-only one that comes through the lung- transmission, helminth, and treatment
larvae penetrate the skin, ancyclodotma duodenal and nectar americans, bedazzles or pyrantel pamoate
intestinal infection larvae enter the blood and encyst in striated muscle cells and inflammation of the muscle. fever vomiting nausea periorbital edema, myalgia- transmission, helminth, and treatment
fecal oral and undercooked pork, trichinella spiralis- bendazoles
neamotes migrate to the blood through intestinal wall causing inflammation and damage the heart and liver and CNS like seizures and coma- transmission, helminth, and treatment
fecal oral, toxacara canis- bensazoles
skin changes, loss of elastic fibers, and river blindness, allergic reaction to microilaria- transmission, helminth, and treatment
nchocera volvulus- female blackly- ivermectin
swelling in the skin, worm in the conjunctiva,- transmission, helminth, and treatment
deer fly, horse fly, mango fly-Loa loa- diethycarbamazine
elepheantitis worms invade lymph nodes and cuase inflammation which can block lymphatic vessels take 9mo-1 year after bite to become symptomatic- transmission, helminth, and treatment
gemale mosquito, wuchereria bancrofti- diethylcarbamazine
intestinal tape worm can cause neuocysticoccis- transmission, helminth, and treatment
taneinia solium- praziquantal- ingesting of larvae encysted in undercooked pork or eggs with human feces
vitamin B12 deficiency causes megaloblatic anemia- transmission, helminth, and treatment
diphyllobothrium datum- parziquantal
hyatid cysts in the liver causing anaphylaxis if the antigens are related. The cyst needs to be injected with ethanol first the kill cysts before removal- transmission, helminth, and treatment
ingestion of eggs from dog or sheep- echinococcus granulosis- albendazole
liver and spleen enlargement fibrosis and inflammation- can lead to squamous cell cancer of the bladder- transmission, helminth, and treatment
schistosoma- snails are host and can penetrate the skin- praziquantal
biliary tract inflammation, pigmented gallstones, cholangiosarcoma- transmission, helminth, and treatment
undercooked fish-clonrchis sinesis-praziquantal
biliary tract disease cholangiosarcoma- what parasite does it
clonorchis sinesis
brain cysts and seizures- what parasite does it
taenia solium
hematuria, squamous cell bladder cancer- what parasite does it
schistosoma haematobium
liver hyatid cysts- what parasite does it
echinococcus granulosis- SW US with dog or sheep with egg shell calcifications can give anaphylaxis
microcytic anemia- what parasite does it
ancylostoma and necator
myalgias, perorbital edema- what parasite does it
trichinella spiralis
perianal puritis- what parasite does it
enterobius
portal hypertension- what parasite does it
schistosoma mansoni, schistosoma japonicum
vitamin B12 deficiecny- what parasite does it
diphyllobothrium latum
mites burrow into the stratum corner and cause puritis cause serpangious burrows in webspace of hands and feet- who and transmission, treatment, what
children and populations, transmission through fomites and skin to skin contact, treat with permethrin cream, washing, drying gall clothing and bedding, scabies
blood sucking insects that prefer to live on clothing. Intense parities pink merciless and papillose commonly in intertriginous regions
lice- pyrethroids, malathion or ivermectin lotion, children get it
exchange of genes between 2 chromosomes by crossing over with regions of base sequence homology
viral recombination
when 1 of 2 viruses that infect the cel has a mutation that results in a nonfunctional protein, the non mutated virus complements the mutated on by making a functional protein that serves both viruses. hepatitis D requires the presence of replicating hep B virus to supply HBsAg, the envelope preteen for HDV.
viral complementation
When virus with segmented genomes, changed genetic material Like the H1N1 flu A pandemic emerged via complex ira reassortment of genes from human, swine, and avian viruses and has potential to cause antigenic shift
viral reassortment
Occurs with simultaneous infection of a cell with 2 viruses. Denim of virus A can be partially or completely coated with surface proteins of virus B and this determines the tropism of the hybrid virus. The progeny from this infection have a type A coat that is only encoded by viral A DNA
phenotypic mixing
what can mediate the species jump between hosts
if the surface glycoprotein changes it mediates the attachment to the host cell, so it can change the type of species it can infect
what kind of response does live attenuated vaccines do
induce humoral and cell mediated response but can sometimes revert back to virulent strain
what vaccines are live
smallpox, yellow fever, rotavirus, chickenpox, Sabin polio, MMR and nasal flu
what kind of immunity does Sabin give compared to Salk
sabin give mucosal immunity through IgA and it is a live attnuated
what are the vaccines with egg allergy
yellow fever and flu
what are the killed vaccines
induce only humoral immunity so might need a booster
which are the killed vaccines
rabies, muscular flu, Salk polio, and HAV
which vaccines are subunit vaccines
HBV and HPV
what DNA viruses are circular
papiloma virus, polyoma, and hepadnavirus
which DNA viruses are single stranded
parvo
which RNA virus is double stranded
Reo
what are the positive RNA viruses
toga, retro, flavi, corona, hepe, and calci and picorna
which types of viruses are infective on their own
positive RNA and double stranded DNA these are able to replicate without host
which DNA virus does not replicate in the nucleus
poxvirus
which RNA virus does not replicate in the cytoplasm
flu and retro
which viruses are naked
papilloma, adeno, parvo, polyoma, calci, picorna, reo hepe
the virus that causes highly ccontagious flesh colored papillose with central umbilication which can be seen on the genitals
poxvirus- molluscum contangiousum
virus family that causes acute and chronic hepatitis that has a reverse transcriptase
HBV hepadena virus which is dsDNA
what cells kill HBV infected hepatocytes and why
CD8 cells kill hepatocytes from MHCI from HBsAg and HbcAg
causes a febrile pharyngitis and acute hemorrhagic cystitis and pneumonia and conjunctivities at daycares, summer caps, and military baracks
adenovirus
causes warts, CIN, cervical cancer and anal cancer- what is the virus and the serotypes that cause each
HPV warts 1,2,6,11; cancer is 16 and 18
progressive multifocal leukoencephalopathy in HIV or MS drugs- would see mental detrioration and ataxia coma
polyomavirus
seen in transplant patients and targets the kidney
BK virus- typically seen in kidney damage and causes complete dysfunction of the kidneys
aplastic crisis in sickle cell patients
parvo B19
slapped cheek rash with high fever
parvovirus
what is the presentation of mother and fetus with congenital parvoB19 infection
adults have symmetric arthralgia and the child has RBC destruction and hydrous fetalis- can have red cell aplasia- questions often mention a school teacher
vesicles on the lips and hard palate with a fever and lymphadenopathy, can be seen on the fingers- what is the virus, family, and transmission and where is it latent
HSV1- respiratory secretion and saliva- sits latent in CNV- intranuclear inclusions
altered mental status, seizures, aphasia and RBC in the spinal tap- what is the virus, family, and transmission
HSV1 temporal lobe encephalitis- personality change plus meningitis
seen as multiple painful ulcerated vesicles on the genitalia- what is the virus, family, and transmission and latent
sexual contact HSV2- stays in the sacral ganglia. Viral meningitis is more common with 2 than 1
causes childhood vesicular illness or in older people it has vesicles in one dermatome only that are paiful- what is the virus, family, and transmission and latency
respiratory secretions VZV- can see inclusions in the keratinocytes and giant cells- sits in dorsal root or trigemninal nerve can use capsaicin to decrease the pain and it decreases substance P
fever, hepatosplenomegaly, pharyngitits, lymphadenopathy, and posterior cervical nodes, increased risk of splenic rupture- what is the virus, family, and transmission and what are the cancers associated with it, and what cells does it effect and how
respiratory secretions or saliva- EBV- can see lymphomas like endemic Burkitt or nasopharyngeal carcinoma in Asians, It infects B cells through the CD21 expansion by CD8 cells and atypical cells appear which are the abnormal T cells called Downey cells. The test is a positive heterophile antibodies
Mono with a negative test and see with pneumonia in transplant patient to aids reitintis which is seen as full thickness retinal necrosis and exam with scar tissue and vascular shutting and absorbed hemorrhage– what is the virus, family, and transmission, characteristic cells and CD4 count for retinitis
CMV- CD4<50, that with gancylcovir have owl eye nuclear inclusions
roseola have high fevers for days then when fever breaks there is a diffuse rash- can have febrile seizures
HHV6 and 7
dark violaceous plaques and nodules that are vascular proliferations can be in lungs and GI- what is the virus, family, and transmission, what patients get it, and what are the lesions look like
HHV8 Kaposi sarcoma- vascualr neoplasm with spindle cells with atypia and blood vessel proliferation and RBC with hemosiderin deposits and bloody diarrhea
what is the Tzanck test for
HSV it is from an opened skin vesicle to look for multinucelated giant cells
what receptors does EBV use
Cd21
what receptors does HIV use
CD4, CXCR4, CCR5
what receptors does rabies use
nicotinic AchR
what receptors do rhino virus use
ICAM-1
cause of fatal diarrhea in children- family and name
rotavirus and reovirus
causes enteritis and anterior horn paralysis
poliovirus-picorna
aseptic meningitis
echo, picorna
causes the common cold
rhino picorna
aseptic meningitis, ulcers on the soft palate and hangs, myocarditis, pericarditis
coxsackievirus, picorna
acute viral hepatitis
picorna HAV- RNA virus
causes hepatitis in pregnant indian women
HEV- hepevirus
viral gastroenteritis with vomitting and diarrhea on a cruise ship
norovirus calcivirus
causes chronic hepatitis from sex and IV drugs- and why is it highly variable
it has no 3’-5’ exonuclease activity- flat- HCV
what mosquito give the virus that has black vomit
aedes and it is yellow fever-flavi
what mosquito carries fever rtetroorbital pain, joint and bone pain, and can have worse symptoms with reinfection because of increased immune response
aegypti- Dengue- flavi
birds are the resovoir for this with humans as the dead end host, and can have a high fever and flu like illness that becomes neurological in 10% of cases with paralysis
WNV- flavi
what are the retroviruses
HTLV and HIV
what are the corona viruses
common cold and SARs and MERS
what is the orthomyxovirus and its special property
flu segments
croup, bronchiolitis in babies, and measles, and mumps- virus, family and specific names of the first two
paramyxo- parainfluenza and RSV
what are the viruses under filovirus
marburg and ebola
what are the arena viruses
LCMV and Lass
what are the bunyaviruses
california encephalitits, crimean congo, hantavirus
how is the hanta virus spread and what does it cause
hemorrhagic gever wit hpulmonary edema from rat urine
what is the only virus in the delta family and what does it need to replicate
HDV and HBV
what must negative RNA viruses bring
RNA dependent RNA polymerase
which are the segmented viruses
bunya, orthomyxo, arena, reo
what cells can be seen in a yellow fever infection
councilman bodies which are eosinophilic apoptotic globules on the liver biopsy
winter daycare diarrhea with blunted villi and lose NA and K
rotavirus
what are the two special proteins for the flu and what do they promote
hemagglutinin- promotes viral entry, and neuraminidase promotes progeny vision release
what is the greatest mortality risk with the flu
superinfection of the lungs with s.aureus, s pneuma, and hflu
what is genetic or antigenic shift
reassortment of the viral genome segments so that it can cause a pandemic
genetic drift/antigenic drift
causes epidemics from mutation in hemagglutinin or neuraminidase
H5N1
bird flu- only bird to human currently- gives URI with some GI features
H1N1
swine flue which is 2 swine, 1 bird and 1 human flu plus Gi
fever, postauricular, and lymphadenopathy with fine confluent rash that starts on the face and spreasds out with arthralgia- wha is the disease and what can congenital infection cause- name and family name
togavirus rubella- maternal infection si a lowgrade fever wit hrash and women get arthralgia but the child gets sensorineural deafness, cataracts, and a PDA with a blueberry muffin rash from dermal extra medullary hematopoesis
seal bark cough and steeple on CXR
parainfluenza virus
what do the paramyxoviruses contain
they form syncitia from a surface fusion protein which causes respiratory epithelial cells to fuse and form multinucleate cells
palivizumab
monoclonal antibody against F protein which his used to prevent pneumonia in at risk premature infacts
what are the common summer viruses
enterovirus and WNV
what are the common winter viruses
RSV, rotavirus, flu
Cough, Coryza, and conjunctivitis, Koplik spots are seen which are red spots on blue which center on the gums followed by a rash that starts at head and goes downward. There is giant cells whcich are fused lymphocytes. The rash coalesces- what vitamin should you give, long term outcome, what is the virus and family
measles- rubeola- paramyxovirus- subacute scelrosing pancencephalitis, giant cell pneumonia, give vitamin A
parotitis, orchitis, aseptic meningitis, and pancreatitis- virus and family
mumps and paramyxo
bullet shaped virus, negri bodies, pukinje cells of the hippocampus and cerebellum, variable incubation based on retrograde axonal transport through nicotinic receptors- fever, malaise, agitation, photophobia, hydrophobia, increased salivation, and paralysis, coma death- what animals is it from and what is it
rabies, from skunk, bat, raccoon
targets endothelial cells, phagocytes, hepatocytes, and has an incubation period of 21 days, abrupt flu, diarrhea, vomiting, diarrhea, high fever, DIC hemorrhage shock- transmission, and virus and family
ebola virus, from fomites, secretions, bats, monkeys, filovirus
what does HBV cause that allows it to progress to hepatocellular carcinoma
p53 mutation
what is the highest risk of being a carrier for HBV
vertical transmission
how can you get HAV
shellfish, fecal oral, tavelers, day care
what is the worse prognosis for HDV
superinfection which is a quick seccession infection
what does HBV have an increased risk for besides cancer
polyarteritis nodosa
what are the HBV markers for acute HBV
+HBsAg, and HBeAg with IgM
what are the HBV markers for windo
only anti-Hbe
what are the HBV markers for chronic HBV high infectivity
HbsAg, and HbeAg with IgG
what are the HBV markers for chronic hBV low infectivity
HBsAg, AntiHbe IgG
what are the HBV markers for recovery
Anti-Hbs and AntiHbe
what are the HBV markers for immunized
Anti-Hbs
what is the env for in HIV
gp120 which is for attachment to T cells and p41 which is for fusion and entry
what are the gag proteins in HIV
p24 and p17 which are capsid and matrix proteins
what are the pol proteins in HIV
reverse transcriptase and integrate which can become resistant in long term HAART therapy- these are used to integrate into the host genome
if you are hetero for a CCR5 mutation or homo for CCR5
hetero is slower course and homo is immunity-
what is the standard HIV test
ELISA which is sensitive but wester blot which is specific after but this does not quickly detect infection
quicker HIV test
- test for antigen before antibody is being produced
what does the acute phase of HIV feel like
flu
what does latent HIV feel like
nothing
when do you start getting hIV symptoms
CD4<400
what are the common HIV diseases with CD4<500
candida oral, EBV oral hairy leuko, cherry red angiomatosis (bartonell henselae), kaposi, cryptosporidium diarrhea, or HPV
CD4<200 illnesses HIV
HIV dementia (see microgliosis), JC reactivation (nonenhancing lesion), PJP ground glass
what is the prophylaxis for PJP
TMP-SMX
CD4<100 illnesses HIV
aspergillus (cavitary lesions), cryptococcus, candida esophagitis, CMV retinitis (cheese pizza used gancylcovir), B cell lymphoma (solitary ring enhancing lesion), histoplasma (oval yeast in macrophages, fever, weight loss, fatigue, cough, dyspnea, nausea, vomitting), MAC, too (multiple ring enhancing lesions)
prophylaxis at CD$<200
PJP- TMP-SMX
prophylaxis at CD4<100
toxo- TMP-SMX
prophylaxis at CD4<50
MAC so azithro once a week
rapidly progressive dementia what are all the causes
CJD- from prions which are abnormal aggregates of beta pleated sheets, mad cow which is mainly England, kuru, dura mater transplant
normal flora of the skin
s epidermidis
normla flora and colonized of the nose
staph epi and s aureus
normal flora of the oropharynx
viridans strep
normal flora of the dental plaque
s mutans
normal flora of the colon
bacteriodes fragilis and ecoli
normal flora of the vagina
lactobacillus, ecoli, and bstrep
food poisoning- rice
b. cerus
food poisoning- canned foods or honey
botulism
food poisoning- reheated meat
perfringens- transiet watery diarrhea, delayed onset from spores germination
food poisoning- undercooked meat
ecoli O157H7
food poisoning-poultry, meat, and eggs
salmonella
food poisoning- meats, mayo, custard
s.aureus- preformed toxin
food poisoning- contaminated seafood
HAV if some hepatitis, or vibe parahemoylticus and vulnificans
bloody diarrhea- s shaped or comma shaped
campylobacter
bloody diarrhea- liver abscess with anchovy paste
entomeabea histolytica
bloody diarrhea- with hemolytic uremic syndrome
ecoli 157H7
bloody diarrhea- invades colonic mucosa and from fecal contamination
ETEC
bloody diarrhea- lactose negative, flagella, poultry and eggs
sallmonella
bloody diarrhea- lactose neg, very low dose needed, can cause hemolytic uremic syndrome
shigella
bloody diarrhea- pseudoapendicitis, puppy or pet wit hdiarrhea
yersinia enteroclitica
watery diarrhea- pseudomembranous colitis, clindamycin or ampicillin can be some blood
c diff
watery diarrhea- from contaminated water while traveling
has heat stabile an heat labile toxin- icily travelers
watery diarrhea- from 2 protozoa
giardia and cryptosporidium
watery diarrhea- comma shaped with watery stool can be from seafood
cholera
watery diarrhea- viral causes (3)
rotavirus, norovirus, adenovirus
what are the common causes of pneumonia-neonate
group B strep, ecoli
what are the common causes of pneumonia- children
RSV, mycoplasma, c, trachomatis, c oenumo, s pneumo,
what are the common causes of pneumonia- adults 18-40
mycoplasma, c penumo, s pneumo, flu
what are the common causes of penumo- adults 40-65
s pneumo, h flu, anearobes
what are the common causes of pneumonia- elderly
s pneumo, flu, anearobes, flu, gram neg rods
what are the common causes of pneumonia- alcoholic
klebsiella or anaerobes
what are the common causes of pneumonia- IV drugs
s penumo or s aureus
what are the common causes of pneumonia-aspiration
anearobes
what are the common causes of pneumonia- atypical
mycoplasma, legionella, chlamydia
what are the common causes of pneumonia-CF
pseudomonas, s aureus, s penumo, burkholdera
what are the common causes of pneumonia-immunocompromised
s aureus, enteric gram neg rods, gundi, viruses, PJP
what are the common causes of pneumonia- nosocomial
s aureus, pseudomonas
what are the common causes of pneumonia-postviral
s pneumo, s aureus, h flu
what are the common causes of meningitis in- newborn
group B strep, ecoli, listeria
what are the common causes of meningitis in- children 6mo-6yr
s pneumo, n meningitis, hflu, enterovirus
what are the common causes of meningitis in- children 6-60 year
s penumo, n meingitits, enterovirus, HSV
what are the common causes of meningitis in- over 60 years
s pneumo, gram neg rods, listeria
why does ceftriaxone not cover listeria
altered PBP binding protein
meningitis- gram positive diplococci
strep pneumo
meningitis- gram negative dilpo cocci
neisseria meningitis
meningitis- gram negative coccobacilli
h flu
what is the flow of infection in neisseria meningitidis
pharynx, blood, choroid plexus, then meninges
what are the most common infection leading to brain abscess
strep viridans, s aureus, and usually from a dental infection like abscess,
what is the cause of osteomyelitis in- normal people
staph aureus
what is the cause of osteomyelitis in- sexually active
neusseria gonorhea but septic is still more common
what is the cause of osteomyelitis in- sickle cell disease
salmonella
what is the cause of osteomyelitis in- prostethis joint replacement
staph aureus or epidermidis
what is the cause of osteomyelitis in- vertebral involement
staph aureus, TB
what is the cause of osteomyelitis in-cat and dog bites
pasturella
what is the cause of osteomyelitis in-IV drug abuse
pseudomonas, candida, staph aureus
childhood rashes-oval shaped vesicles on palms and soles and oral mucosa
coxsackie A- hand foot and mouth
childhood rashes- asymptomatic rose colored merciless on the body with high fever, febrile seizures and infants
HHV6- roseola
childhood rashes-begins at his and moves down, rash is proceed by cough, coryza, conjunctivitis and Koplik spots
roseola
childhood rashes-erythematous, sandpaper rash, fever and sore throat
scarlet fever, and strep pyogenes
childhood rashes- vesicular rash begins on trunk, spreads to face and extremities with lesions of different stages
varicella zoster
nosocomial infection: antibiotic use
c diff- disrupt cell membrane- need gloves and gown
nosocomial infection: aspiration secondary to altered mental status or old age
polymicrobial gram negative bactera-
what lobe is affected with aspiration pneumonia if laying down
right middle lobe
what lobe is affected with aspiration pneumonia if sitting up
right upper lobe
nosocomial infection: decubitus ulcers, surgical wounds and drains
staph aureus and anearobes-erythema tenderness, induration and drainage from surgical site
nosocomial infection: intravascular catheters
staph aureus, staph epi, enterobacter or pseudo
nosocomial infection:mechanical ventilation, endotracehal tube
pseudomonas, kleb, acinetobacter, s aureus- sputum with sweet odor
nosocomial infection: renal dialysis unti needlestick
HBV
nosocomial infection:urinary catheterization
ecoli, kleb, proteus- dusuria, leukocytosis, flank pain, costovertebral angle tenderness
nosocomial infection: water aerosols
legionella, signs of pneumonia, GI nausea vomiting, neurologic abnormalities
what meningitis microbe colonizes the nasopharynx
h flu
asplenic patient with infection
s pneumo, h flu, n meninges
branching rods in oral infection with sulfur granules
actinomyces
chronic granulomatous disease- infection
catalase postive organism like s aureus
currant jelly sputum
klebsiella
dog or cat bite
pasturella
facial nerve palsy
lyme disease
fungal infection of diabetic or immunocompromised
muco or rhizopus
heath care provider needlestick
HBV
neutropenic patent with fungal infection
candida or aspergillus
organ transplant recpient infection
CMV
PAS positive
tropheryma whipplei
pediatric infection of epiglotitis
h flu
pneumonia in cystic fibrosis or burn patient
pseudomonas
pus, empyema, and abscess
staph aureus
rash on hands and feet
coxsackie A, treponema pallidum, rickettsia rickettsii
sepsis/meingitis in newborn
group B strep
surgical wound infection
staph aureus
traumatic open wound
clostridium perfringens
what is TB prophylaxis
isoniazid
what is TB treatment
rifampin, isoniazid, pyrazinamide, ethambutol
whats prophylaxis for MAC
azirhtomycin
what is the treatment for leprosy
dapsone, rifampin, and sometimes clofazimine
zero order elimination
rate of elimination is constant regardless of Cp.
what are the examples of zero order elimination
phenytoin, ethanol and aspirin
what is first order elimination
rate of elimination is directly proportional to the drug concentration. Constant fraction of drug eliminated per unit time. It applies to most drugs
weak acids are trapped in the urine with what? and what are drug examples of this
trapped with bicarb. It is phenobarbitol, methotrexate, and aspirin
weak bases are trapped in the urine with what and what are the drug examples
it is trapped with ammonium chloride and it is amphetamines, TCAs
What are the reactions of Phase 1 metabolism
reduction, oxidation, hydrolysis with P450
what kind of metabolites does phase 1 reactions produce
still somewhat active metabolites
what kind of metabolites does phase 2 reactions produce
methylation, glucordination, acetylation, sulfonation
what kind of metabolites does Phase 2 reactions produce
inactive metabolites
what patients have increased drug side effects
decreased metabolism because of slow acetylation
what is efficacy
maximal effect a drug can produce. Unrelated to potency. It is basically the Vmax
what is the change in efficacy for a full agonist and partial agonist
The partial agonist has decreased efficacy
what is potency
amount of drug needed for a given effect. It is represented by EC50 which is the Km.
As the EC50 decreases, the potency does what
increases because you don’t have yo give as much drug
what is the therapeutic index
it is the median toxic dose over the median effective dose
what drugs have a low therapeutic index
seizure drugs, digoxin, warfarin, lithium, theophylline
What are nicotinic Ach receptors- what is the type of receptor and where are they found
it is a ligand gated Na/K channels. They are on autonomic ganglia and NMJ and skeletal muscle.
What are the muscarinic Ach receptors- what type of receptor are they and where are they found
G protein coupled receptors and usually act through second messengers. They are found in heart, smooth muscle, brain, exocrine glands, and on sweat glands
Left axis deviation of the heart
inferior wall MI, left anterior fasicular block, left ventricular hypertrophy, LBBB
right axis deviation of the heart
right ventricular hypertrophy, acute right heart strain like a PE, left posterior fasicular block, RBBB
if T wave is peaked
hyperkalemia
flat T wave
decreased K
U wave
depolarization of papillary muscle- increased Ca or decreased K
what induces torsades
class Ia and III antiarrythmics, macrocodes, haloperidol, TCAs, ondansetron, decreased K and MG
how to treat torsades
magnesium sulfate
Romano Ward syndrom
AD- cardiac defect in ion channels leadsing to spontaenous torsades and surdden cardiac death
Jervell and LAnge Neilsen syndrome
dfeective K channel leads to tornadoes risk and long QT with deafness
Brugada
Asian makes AD with pseudo RBBB and ST elevations with increased risk of tach and SCD.
WPW
abnormal accessory pathway in the atria to ventricle to the bundle of Kent and it bypasses the AV node leading to ventricles begin to partially deploy earlier and shortened PR interval- SVT
carotid sinus what nerves does it use
afferent is glossopharyngeal and efferent is vagus
arotic receptors what nerves does it use
both are vagu
ANP does waht
increase in response to increased blood volume and causes diuresis through decreased NA absorption at CT and constrict efferent and dilated afferent to increase GFR.
what increases the effect of ANP
neprilysin stops its degradation
BNP does what
it is in response to tension and it is the test for heart failure
what is the reaction of the carotid to decreased BP
firing decreases and decreased PNS and increased SNS so increased a1 and B1 to increased BP and HR
what is the reaction to increased BP
increased firing so increased PNS tone through the vague and glossopharyngeal
what are the drivers of the central chemoreceptors
PCO2 and pH
what are the drivers of peripheral chemoreceptors
PCO2, PO2, and Ph
what happens to chemoreception in COPD
there is blunted response to Pco2 and so O2 decreasing becomes the driver of breathing response so it becomes the responsibility of the peripheral chemoreceptors
ASD murmur
wide fixed split S2 and flow over RH
congential rubella heart issue
PDA or pulmonary stenosis
down heart defect
endocardial cushion defect
marfan heart issue
myoxmatous degeneration of the media of vessels. MVP, thoracic aortic aneurysm, dissection, aortic regurg
turner heart issues
bicuspid aortic valve, coarctation of the aorta
Williams heart issues
supravalvular aortic stenosis
Digeorge syndrome heart issue
truncus or get of Fallot
which vessels are hit first with atheroscelrosis
abdominal aorta, coronary vessels, popliteal and carotid
medial calcific scelrosis
calcified internal elastic lamina and media of arteries still but not obstructed looks like a pipestem
what areas are more effects by atherosscelorsis and why
low flow areas near branch points because there is more accumulation
pathogenesis of atheroscelorsis
endotherlila dysfunction, macrophage and LDL accumulation, foam cells, fatty streak, smooth muscle migration proliferation and em deposition, fibrous plaque, complex atheroma
traumatic aortic rupture
deceleration injury near the aortic isthmus in proximal descending aorta distal to the left subclavian because of insertion of a tendon there
standford A aortic dissection
ascending aorta, near sinotubular junction, aortic regard and tamp anode with valvular issues- surgery
stanford B aortic dissection
descending aorta and arctic arch by left subclavian treat with beta blockers
what things can cause prinzmetal angina
can be secondary to spasm- smoke, coke, triptans
coronary steal syndrome
distal to cornoary stenossis, vessels are dilated and if give dilators then the already dilated vessels in well perused areas get blood furthering the ischemia of the necrotic tissue
chronic ischemia of the heart can lead to
HF
STEMI is what
full wall thickness- st elevation
NSTEMI
only subendocardial ischemia with ST depression
