Blue Flags Flashcards
incidence
number of new cases/number of people at risk
prevalence
number of existing cases/total number of people in pulation
what does short disease duration do to incidence and prevalence
they should be roughly equal
what does long disease duration do to incidence and prevalence
prevalence increases over incidence because of the increased number of cases
type 1 error
false positive
type 2 error
false negative. related to the statistical power
t test
checks the difference between 2 means
ANOVA
checks the differences between the means of 3 or more groups
Chi-square
checks differences between 2 or more percentages or proportions or categorical outcomes
informed consent
disclosure of pertinent information, ability to comprehend the information, capacity o make own decisions, voluntary freedom from coercion, understand proposed treatment, outcomes, alternative options, risks and benefits
patient is non adherent
determine reason for non adherence and determine the willingness to change
desire unessecary procedure
understand why they want the procedure and address underlying concern, Do not reduce or refer to another
patient struggles to take medication
provide written instructions, attempt to simplify regiments, use teach back method
family members ask for information about prognosis
avoid discussing issues with relatives without the patients permission
family member asks physician to not disclose the results of the test if the prog is poor because the patient will not handle it well
attempt to identify why they think this information will be harmful to the patient. Explain that the patient has decision making capacity until there is communication otherwise
17 year old girl requests an abortion
require parental consent.
parents want girl to give up child of 15 yo pre girl
girl has rights about the child. discuss options if requested
terminally ill patent requests physician assisted suicide
refuse involvement of the physician but can prescribe medically appropriate analgesics that coincidentally shorten the patients life
patient is suicidal
assess the seriousness of the threat suggest the patient remain in the hospital and if not make them stay
patient thinks you’re attractive
ask direct, close ended questions and use a chaperone. NEVER DATE
a woman who had a mastectomy says she now feels ugly
find out why the patient feels this way
patient is angry about wait time
acknowledge the anger and do not take it personally. Do not explain the delay
patient is upset with how they were treated by another doctor
suggest that the patent speak directly to that physician directly about the concerns
an invasive test is performed on the wrong patient
inform the patient of the mistake
requires a treatment not covered by insarance
never delay or limit care based on this. Discuss all options even if they are not covered
a boy loses his sister and now feels responsible
5-7 year olds understand death is permanent and all life function is gone. Proved a direct concrete description of his sisters death. Normalize fear and feelings and encourage lay and healthy coping behavior
common causes of death by age- under 1
congenital malformations, Preterm birth, SIDS
common causes of death- 1-14 years
unintentional injury, cancer, congenital malformation
common cause of death 15-34 years
unintentional injury, suicide, homicide
common cause of death 35-44
unintentional injury, cancer, heart disease
common cause of death 45-64
cancer, heart disease, unintentional injury
common cause of death 65+
heart disease, cancer, COPD
hospital conditions with high readmission rate- medicare
congesitive HF, septic, pneumonia
hospital conditions with high readmission rate- medicaid
mood disorder, schizophrenia, DM
hospital conditions with high readmission rate- private insurance
chemo radiation, mood disorder, complications of surgery
hospital conditions with high readmission rate- uninsured
mood disorder, alcohol related, DM
delirium symptoms
waxing and waning level of consciousness with acute onset, rapid decrease in attention span and arousal. Disorganized thinking, hallucinations, altered sleep, cognitive dysfunction- slowing EEG
delirium causes
CNS disease, UTI, trauma, substance abuse, withdrawal, metabolic or electrolyte disturbance, hemorrhage, urinary or fecal retention. can be medication related in the elderly especially anticholinergics
delirium treatment+ what not to give
use haloperidol and treat underlying condition. Do not give benzos because this can worsen it in the elderly unless its for alcohol withdrawal
dementia
decreased intellectual function without affecting consciousness. Characteristic memory deficits, apraxia, aphasia, agnosia, loss of abstract thought, behavioral/personality changes, impaired judgement. Can develop delirium.
dementia causes- irreversible
AD, Lewy body dementia, HD, Pick, cerebral intact, Mad cow, chronic substance abuse
reversible causes of dementia
hypothyroid, dpression ,B12 def, NPH, neurosyphillus, hydrocephalus
EEG in delirium vs. dementia
Delirium has a diffuse slowing EEG and dementia has a normal EEG
major depression how long before diagnossi
need 2 weeks for symptoms
major depression treatment
CBT and SSRI
major depression symptoms
depressed mood, sleep disturbance, loss of interest, guilt or feelings of worthlessness, energy loss and fatigue, concentration problems, appetite/weight changes, psychomotor retardation or agitiation, suicidal ideations
depression sleep changes
decreased REM latency, decreased slow wave sleep, increased REM early in the cycle, increased REM overall, repeated nighttime awakening, early morning awakening
dysthymia
persistent depressive disorder- mild depression lasting at least two years
atypical depression
mood reactivity- able to cheer up, reversed vegetative, hypersomnia, hyperphageia, leaden paralysis, interpersonal rejection sensitivity
Cluster A
paranoid, schizoid, schizotypal
pervasive distrust and suscpiciousness; projection is the major defense mechanism
paranoid
voluntary withdrawal from social situations, limited emotional expression, content with social isolation
schizoid
eccentric appearance, odd beliefs, or magical thinking, awkward in relationships
schizotypal
Cluster B
antisocial, borderline, histrionic, narcissitic
cluster C
avoidant, OCPD, dependent
disregard for and violation of rights or others, criminality, M>F, goes by another name before the age of 18
antisocial
unstable mood and interpersonal relationships, impulsive, self-mutiliation, suicidal, sense of emptiness, splitting
borderline
excessive emotionality and excitability, attention seeking, sexually provocative, overly concerned with appearance
histrionic
grandiose, sense of entitlement, lacks empathy and requires excessive admiration, often demands the best and reacts with rage to criticism
narcissistic
hypersensitive to rejection, socially inhibited, timid, feelings of inadequacy, desires relationships with others
avoidant
preoccupation with order, perfectionism and control. behavior bothers others but not self
OCPD
submissive, clingy, excessive need to be taken care of, exceedingly low self-confidence
dependent
Fab region
fragment antigen binding- determines the unique antigen binding pocket only 1 antigen per B cell
Fc region
constant region, carboxy terminus, complement binding, carbohydrate side chains
Generation of antibody diversity
random recombination of VJ and D genes which are for the chains. The random addition of nucleotides to a DNA during recombination by terminal TDT determine this and then there is a random assignment of light chains to heavy chains
generation of antibody specificity
somatic hypermutation and affinity matuation- variable switching, isotype switching
what can antibodies do
prevent bacterial adherence (neutralization), opsonixation (promotion of phagocytosis), complement activation activates C3B and the mac complex
what antibody is the most abundant in the serum
IgG
what antibody fixes complement, crosses placenta, opsonizes bacteria, and neutralizes bacterial toxins and viruses
IgG
what antibody prevent attachment of bacteria and viruses to mucus membrane
IgA
what antibody is produced by the GI tract and protects against gut infecttions
IgA
what antibody is released into the secretions like tears, saliva, mucus and breast milk
IgA
what antibody is the first response to an antigen
IgM
what antibody fixes complement but does not cross the placenta
IgM
Pentamer antibody
IgM
what antibody is found on the surface of B cells
IgD
what antibody binds mast cells and basohils
IgE
what antibody cross links when exposed to allergen mediating the type I HSN through release of histamine
IgE
what antibody mediates defense against worms
IgE
recurrent bacterial and enteroviral infections like giardia and increased encapsulated infections. There are no B cells in the peripheral blood and decreased Ig of all classes. No tonsils or lymph nodes
defect in BTK which leads to no B cell maturation and X linked recessive called Bruton agammaglobulinemia
Airway and Gi infections with atopy, and autoimmune and anaphylaxis to blood products. Decreased IgA and normal others. Celiac is common. Recurrent sinus infections
selective IgA deficiency- must wash red blood cells
20-30 yo patient with increased autoimmune diseases, bronchiectasis, lymphoma, sinopulmonary infections. decreased plasma cells and decreased immunoglobulins
defect in B cell differntiation- Common variable immunodeficiency
Tetany, hypocalcemia, recurrent viral and fungal infections, conotruncal abnormalities like tetralogy of Fallot and truncus arteriosis. Decreased T cell and PTH, decreased Ca. absent thymic shadow,
Thymic aplasia like Digeorge. It is from 3 and 4 pharnygeal pouch failure
disseminated mycobacterial and fungal infections may present after administration of BCG (Tb vaccine), decreased IFN gamma, decreased Th1 response
IL12 deficiency
coarse facies, cold staph abscesses, retained primary teeth, increased IgE, dermatologic problems. decreased interferon gamma
deficiency of Th17 cells so impaired recruitment of neutrophils to sites of infections- autosomal dominant hyper IgE syndrome
noninvasive candida infections of the skin and mucous membranes. Absent invert T cell proliferation response
T cell dysfunction- chronic mucocutaneous candidiasis
failure to thrive, diarrhea, thrush, recurrent infections like PJP. treated with Bone marrow transplant. Decreased T cell receptor excision circles, absence of thymus shadow, no germinal centers, and no T cells.
SCID- defective IL2R gamma chain. Adenosine deaminsase deficiency
cerebellar defects, spider angiomas, IgA deficiency- increased AFP, decreased IGA, IGG, IGE. lymphopenia and cerebellar atrophy
defect in ATM gene- failure to repair DNA double strand breaks- arrest the cell cycle- Ataxia telangactasia
severe pyogenic infections early in life with opportunistic infections like PJP, cryptosporidium, and CMV. Normal IgM but decreased IgG, A, and E
defective CD40L on Th cells that impaired class switching- hyper IgM
Thrombocytopenia, eczema, recurrent infections, increased autoimmune disease- increased IgE and IGA but decreased G and M
WAS mutation so T cells are unable to reorganize actin cytoskeleton- Wiskott Aldrich
Recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, and delayed cord separation. increased neutrophils not in the infection site
Defect in LFa1 so impaired migration and chemotaxis and is autosomal recessive- Leukocyte adhesion deficiency
recurrent staph, strep, and albinish, peripheral neuropathy, progressive neurodegeneration, infiltrative lymphocytosis, griant granules in the granulocytes and platelets. pancytopenia, mild coagulation defects
Chediak Higashi Syndome
increased catalase positive infections- nocardia, pseudomonas, listeria, aspergillum, candida, icily, staph, serration, b coppice, h pylori- nitroblue is not reduces
chronic granulomatous disease from NADPH oxidase deficiency
deficiency leads to chalices with inflammation of lips scaling and fissures of the corners of the mouth and corneal vascularization-
B2 riboflavin
what does B2 do
component for redox reactions
deficiency of this leads to glossitis, severe leads to pellagra, with diarrhea, dementia, and dermatitis with broad collar rash with hyper pigmentation of the skin
niacin deficiency
what is Hartnup disease
AR recessive deficiency ot tryptophan and so there is aminoacidura and decreased gut absorption and this means decreased niacin
excess of this leads to facial flushing, hyperglycemia and hyperuriciemia
this is niacin
what can niacin trat
lower levels of VLDL and raises levels of HDL because its part of NAD and NADP
deficiency causes dermatitis, enteritis, alopecia, and adrenal insufficiency
this is from B5 or pantothenic acid
deficiency leads to convulstiona, hyper irritability, peripheral neuprpathy, sideroblasts dur to impaired hemoglobin- and causes
B6 deficiency- isoniazid and oral contraceptives
function of B6
used for NT
deficiency causes dermaittis, alopeica, enteritis- eats lots of egg whites
biotin of B7- ued for putuvate carboxylase, acetyl coz to alony coa, oropionyl coa and methylamolnyl coa
deficiency leads to macrocytic megalibalstic anemia, hyperhsegmented polymophonuclear cells, glossitis, no neurology symptoms. increased homocysteine. see in what two risk groups
folic acid or B9- seen in pregnancy and alcoholics
deficiency of microcytic and megaloblastic anemia, hypersegmented PMN< prothesis, subacute combined degeneration, corticospinal tracts, and abnormal myelin. increased homoystein and methylmalonic acid. Prolonged deficiency leads to nerve damage- what can cause it
stored in the liver and taken up in the terminal ileum, malabortiptio from sprue or enteritis, liver fluke, pernicious anemia, gastric bypass crowns or vegans
deficiency swollen gums, brusing, petichaie, hemarthorosis, anemai, poor wound healing, perifollicular and subperiosteal hemorrhages with corkscrew hairs
cannot hydroxylate proline and lysine for collagen synthesis- vitamin C
excess is vomiting, nausea, fatigue, calcium oxalate nephrolithiasis, and increased risk of iron toxicity
vitamin C
deficiency- rickets ostomalacia, and tetany from the hypocalcemia
D- breastfed do not get it oral low sun exposure, pigmented skin
what enzyme activates vitamin D
alpha 1 hydroxylase
excess ledas to hypercalcemia, hypercalciuria, loss of appetite, stupor, and grnaulomas
vitamin D
def- hemolytic anemia, acanthocytosis, muscle weakness,posterior collumn and spinocerebellar tract demyelination- no megaloblastic aneia or increased methylamlonic acid- looks the same as B12 def
vitamin E
what does vitamin E do
it is an antioxidnat
def leads to neonatal hemorrhage with increased PT and PTT but normal bleeding time. neonatal have sterile Gi so cannot make it yet or prolonged antibiotics
vitamin K
what does fetus look like with K def
intracranial pressure and refused vaccin
deficiency leadsto delayed wound healing, hypogonadism, decreased axillary hair, dysgeusia, anosmia, acrodermatitis enteropathica- why and what
zinc can be from small intestine malabsortion
protein malnutrition resulting in skin lesions, and edema from decreased plasma oncotic pressure.
Kwashiorkor
total calorie malnutrition resulting in emaciattion like tissue and muscle wasting and loss of subcutaneous fat
marasmus
rate limiting enzyme for glycolysis
phosphofructokinase 1
rate limiting enzyme for gluconeogenesis
Fructors 1 6 bisphosphate
rate limiting enzyme for TCA
isocitrate dehydrogenase
rate limiting enzyme for glycogenesis
glycogen synthase
rate limiting enzyme for glycogenolysis
glycogen phosphorylase
rate limiting enzyme for HMG shunt
G6PD
rate limiting enzyme for de novo pyrimidine synthesis
CPS2
rate limiting enzyme for de novo purine synthesis
PRPP amidotransferase
rate limiting enzyme for urea cycle
CPS1
rate limiting enzyme for fatty acid synthesis
acetyl coa carboxylase
rate limiting enzyme for fatty acid oxidation
carnithine acyltransferase I
rate limiting enzyme for ketogenesis
HMG CoA synthase
rate limiting enzyme for cholesterol synthesis
HMG reductase
when is hexokinase used and what are its enzymatic properties
it is in most cells and it has a low km but high affinity but low Vmax
when is glucokinase used and what are its enzymatic properties
only in the liver and on Beta cells of the pancreas. It is insulin dependent. Need a lot of glucose to use it, but it has a high km but high Vmax so very efficient
derivatives of phenylalanine
tyrosine, thyroxine, dopa, melanine, dopamine, NE, epi
derivatives of tryptophan
niacin, serotonin, melatonin
derivatives of histidine
histamine
derivatives of glycine
porphyrin, heme
derivatives of glutamate
GABA and glutathione
derivatives of arginine
creatine, urea, nitric oxide
severe fasting hypoglycemia, increased glycogen in the liver, increased blood lactate, increased triglycerides and increased uric acid and hepatomegaly- what is the deficiency, enzyme, and treatment
Von Gierke disease- glucose 6 phosphatase deficiency- treat with frequent glucose and corn starch and avoid galactose and fructase- impaired gluconeo and glycogenolysis
patient has cardiomegaly, hypertrophic cardiomyopathy, exercise intolerance and some systemic symptoms-what is the deficiency, enzyme, and treatment
lysosomal alpha 1,4 glucosidase with alpha 1,6 activity- defiency- Pompe trashes the pump- heart, liver, and muscle
patient has normal blood lactate but accumulate of limit dextrin in the cytosol- some hypoglycemia-what is the deficiency, enzyme, and treatment
defieincy in the deb ranching enzyme- alpha 1,6 glucosidase- gluconeogenesis is intact will see branch end points
paient has increased glycogen in the muscle, but the muscle cannot use it. they have painful muscle cramps, red urine with strenuous exercise, and arrthymia from electrolyte issues- have some second wind from increased muscle blood flow-what is the deficiency, enzyme, and treatment
deficient in glycogen phosophorylase and myophosphorylase- McArdle- blood glucose is unaffected
episodic peripheral neuropathy, angiokeratomas, hypohidrosis, and progressive renal failure and heart disease later in life-what is the deficiency, enzyme, and treatment, and what accumulates
Fabry disease-deficient in alpha galactosidase A and accumulate ceramide trihexosidase- it is the only one that is x linked recessive
hepatosplenomegaly, pancytopenia, osteoporosis, aseptic necrosis of the femur, bone crisis, lipid laden macrophages with tissue paper-what is the deficiency, enzyme, and treatment, and what accumulates
Glucocerbrosidase- beta glucosidase- build up of glucocerebroside- Gaucher
progressive neurodegeneration with hypotonia, hepatosplenomegaly, foam cells, and cherry red macula-what is the deficiency, enzyme, and treatment, and what accumulates
sphingomyelinase deficiency with sphingomyelin increased- Nieman Pick
progressive neurodegeneration, developmental delay, cherry red macula, onion skin lysosomes, no hepatosplenomegaly-what is the deficiency, enzyme, and treatment, and what accumulates
hexosaminidase A build uo of GM2 ganglioside
peripheral neuropathy, developmental delay, optic atrophy, globoid cells and seizures-what is the deficiency, enzyme, and treatment, and what accumulates
Krabbe- galactocerebrosidase
central and peripheral demyelination with ataxia and dementia–what is the deficiency, enzyme, and treatment, and what accumulates
Metachromic leukodystrophy- arylsulfatase A
developmental delay, coarse face and joints, airway obstruction, corneal clouding, and hepatosplenomegaly–what is the deficiency, enzyme, and treatment, and what accumulates and inheritance
Hurler- alpha L iduronidase- heparin and dermatin sulfate build up- AR
aggressive behavior, no corneal clouding, coarse face and joint pain-what is the deficiency, enzyme, and treatment, and what accumulates and inheritance
Hunter- iduronate sulfatase- heparin and dermatin sulfate- XR
weakness hypotonia and hypoketotic hypoglycemia-what is the deficiency, enzyme, and treatment, and what accumulates
carnithine deficiency- inherited defect in transport of LCFA into the mitochondria leading to toxic accumulation
patient has vomiting, lethargy, seizures, coma, liver dysfunction with hypoketotic hypoglycemia–what is the deficiency, enzyme, and treatment, and what accumulates
avoid fasting- decreased ability to break down fatty acids- medium chain acyl cos dehydrogenase deficiency
what leads to an increased risk of UTI
vesicoureteral reflux
what is there determining risk factor for UTI from cathertization
the duration of catheterization
what is the leading cause of UTI
ecoli
what is the second leading cause of UTI in sexually active women
staph spare which is novobiocin resistant
what is the cause of UTI that has large mucoid capsule and colonies that are viscous
klebsiella
what are UTI that have red pigment and drug resistant
serratia
UTI with swarming motility and produces urease
proteus
UTI with blue green pigment and fruity odor- long term indwelling catheter
pseudomonas
no inflammation, but thin white vaginal discharge with dish ordor and clue cells
gardenerlla- treat with metronidazole
strawberry cervix, forthy yellow green, foul smelling discharge, motile
trichomonas- metronidazole
inflammation with thick white cottage cheese, with pseudohyphae
candida and use azoles
congenital infection: bug, and transmission- chorioretinitis, hydrocephalus, and intracranial calcifications and blueberry rash
cat feces, toxoplsmosis
congenital infection: bug, and transmission, and mom- abnormalities of the eye, including catarachts, deafness, PDA, and blueberry mffin rash
respiratory droplets, maternal has arthralgia, lymphadenopathy- rubella,
congenital infection: bug, and transmission, and mom- blueberry rash, hearing loss, seizures, poetical rash, and periventricular calcifications
sexual contact or organ transplant, mono illness in mom- CMV
congenital infection: bug, and transmission, and mom- recurrent infections, chronic diarrhea
sexual contact or needlestick, low CD4 count, and HIV
congenital infection: bug, and transmission, and mom- encephalitis and vesicular lesions
skin mucus membranes, asymptomatic in the mom or some ulcerated lesions HSV 2
congenital infection: bug, and transmission, and mom- hydrops detalis, facial notched teeth, and saddle nose, saber shins, deafness
syphilis- from sex- chancre or disseminated in stage 2
STI lesion- painful genital ulcer with exudate and inguinal adenopathy
chancroid- haemophilus ducreyi
STI lesion- urethritis, cervicitis, epiddimitis, conjunctivitis, reactive arthritis, PID
chylamydia D-K
STI lesion- warts and koilocytes
condylopma accumoinata- HPV
STI lesion- painful penile, vulvar, and vercival lesions, ulcers, systemic symptoms such as fever headache, myalgia
HSV2
STI lesion- urethritis, PID, prostatitis, epidydimitis, arthritis, creamy purulent discharge
gonorrhea
STI lesion- jaundice
HBV
STI lesion- infection of lymphatics, painless genital ulcers, painful lymphadenopathy, buboes
lymphogranuloma venereum- C trachomatis L1-L3
STI lesion- painless chancre
trponema pallidum- primary syphillus
STI lesion- fever, lymphadenopathy, skin rashes, condyloma lata
secondary syphilis
STI lesion- gummas, tabes dorsalis, general paresis, aortitis, argyll robertson pupil
tertiary syphilis
STI lesion- vaginitis, strawberry cervis, motile on wet prep
trichomonas
cervical motion tenderness, purulent discharge, salpingitis, hydrosalpinx, and tubo-ovarian abscess
PID
what can happen from PID
ectopic pregnancy, pelvic pain, adhesions
what is Fitzhugh Curtis Syndrome
infection of liver capsule and violin string adhesions of peritoneum to liver
what is the Michaelis Menten- what is K, an what is Vmax
Km is inversely related to the affinity of the substrate, so the lower the Km the tighter the binding. The Vmax is directly proportional to to the enzyme concentration. The max is when it is saturated.
what changes with Michaelis-Menten if there is a competitive inhibitor
It means that the vmax stars the same, but the Kmax is higher,
what changes with Michaelis-Menten if there is a non competitive inhibitor
The vmax decreases
In regards to the Lineweaver Burke plot- what is the y axis and x axis
yaxis is 1/V and x axis is 1/concentration of substrate
In regards to Michaelis-Menten- what is the y axis and x axis
y axis is V and x axis is concentration of substrate
In regards to the Lineweaver Burke plot- what happens if the V max decreases
The y intercept is increased as max decreases
if there is a reversible competitive inhibitor, what is the effect of Vmax and Km
vmax is unchanged and Km increases
If there is a irreversible competitive inhibitor, then there is
a decrease in Vmax and KM is unchanged
if there is a noncompetitive inhibitor then there is
a decrease in Vmax and Km is unchanged
Which inhibitor can be overcome with increased substrate
the reversible competitive inhibitor can be overcome with substrate
If there are curves then how do you calculate the bioavailability
F=(area under curve oral x IV)/(area under IV curve x oral dose)
what happens with oral bioavailability- why does it decrease with oral
High first pass metabolism through the liver leads to decreased serum drug
where is absorption of rectum based on pectinate line
if below the pectinate line, it can increase bioavailability because of systemic circulation. If it is above the pectinate line, it can go through portal circulation so there is decreased drug
What is bioavailability of IV
it is 100%
What is the volume of distribution and formula
It is the theoretical volume occupies by the total amount of drug in the body relative to plasma concentration. Apparent Vd of plasma portion bound drugs can be altered by the liver and kidney disease, so decreased binding to protein leads to increased Vd. Vd= amount of drug in body/plasma concentration and Vd=drug in IV/ drug in plasma
what is the Vd in the blood
low Vd because large charged molecules stay bound
what is the Vd in the ECF
it is medium, and small hydrophobic molecules
what is the Vd in all tissues including fat
It is high and small lipophilic molecules attached to protein
clearance of a drug- definition and formula
the volume of plasma cleared of drug per unit time. Clearance may be impaired with defects in cardiac, hepatic, or renal function. Clearance= rate of elimination of drug/plasma concentration of the drug=Vd x Ke or Cl=.7Vd/t.5
half life definition and formula
the time required to change the amount of drug in the body by 1/2 during elimination. t.5= .693Vd/Cl
what is the percent eliminated at 1,2,3,4 half lives
1 is 50%, 2 is 75%, 3 is 87.5%, and 4 is 94%
what is the equation for loading dose
Css x Vd= loading dose
what is the equation for maintenance dose
MD= Css x Clearance
what does renal and liver disease do to maintenance dose
it decreases the maintenance dose and doesn’t change the loading dose
what is the additive effect of drug interactions
effect of substance A and B together is equal to the sum of their individual effects
what is the permissive effect of drug interactions
presence of substance A is required for the full effects of substance B
what is the synergistic effect of drug interactions
effect of substance A and B together is greater than the sum of their individual effects
what is the tachyphylactic effect of drug interactions
acute decrease in response to a drug after initial or repeated administration.
with a competitive antagonist, what happens to the potency and efficacy and an example
The curve shifts right, so the potency is decreased but there is no change in efficacy because it can be overcome which the addition of substrate- diazepam and flumazenil
with a noncompetitive antagonist, what happens to the potency and efficacy and an example
It shifts the curve down, so there is decreased efficacy that cannot be overcome with increased substrate. An example would be- NE and pehnoxybenzamine
with partial agonist, what happens to potency and efficacy and an example
It acts at the same site as full agonist, but with lower maximal effect, so decreased efficacy and potency is independent- morphine and buprenorphine.
what increases SV
increased contractily, increased preload, and decreased after load. a failing heart has decreased SV
what ions increase contractlity
increased intracellular Ca and decreased extracellular NA- digitalis exploits this by raising the intracellular NA and Ca but working on the NA Ca exchanger.
what do venodilators do to preload
decreased preload
draw a pressure volume loop and label
yay
S1 heart sound
M and T close
S2
a p close
S3
increased with increased filling pressures like mitral regard or heart failure or dilated ventricles
S4
heart as an atrial kick in late diastole from the atria having to contract more forcefully against the hypertrophied ventricles
JVP a wave
atrial contraction
JVP x wave
atrial relaxation
JVP c wave
RV conration
JVP v wave
is the RAP increasing from filling
JVP y wave
the RV is filling from the RA
what does handgrip do to murmurs
it increases the after load which increases mitral regurg, and aortic regard and creates a later MVP click
what does valvalva do to murumurs
decreases the preload to it increases hypertrophic cardiomyopathy
what does rapid squatting do
it increases venous return, preload and after load which increases the intensity of AS and decreases the hypertrophic cardiomyopathy murmur
crescendo decrescendo murmur systolic- delayed pulses, syncope, angina, dypnea-
AS
what is AS usually from
calcification of a bicuspid or normal valve
holosystolic hugh blowing murmur
regurg
holosystoic high pitched blowing murmur that radiates towards the axilla- what is it and whats it from
MR from ischemic heart disease, MVP, Lv dilation
holosystolic high pitched blowing murmur that is in the right sternal border
causes by RV dilation- TR
late systolic crescendo murmur with mid systolic click. due to sudden tensing of the chordae tendinae- heard over the apex. Loudest just before S2- what and why
MVP from myxomatous degeneration from connective tissue disorder, and rhematic fever or chord rupture
holosystolic harsh murmur over the right sternal border
VSD
high pitched blowing murmur in the early diastolic time with head bobbing and wide pp. what and why
it is AR from aortic root dilation from bicuspid aortic valve, rhenmatic never, syphillus, marfan, endocarditis, and leads to let HF
opening snap in diatole and late rumble what and why
MS- the S2 and OS correlate with severity and the LA is greater than LVP- it can be from rheumatic fever and lead to LA dilation
continuous machine mumur on S2
PDA can be from congenital rubella and closes with indomethacin and prostaglandin E keeps it open
what does increased serotonin do to the heart
it increases the fibroblasts which leads to increased fibornous tissue leading to tricuspid regard and pulmonary valve isses
what can AS go to if it decompensates
can go to HF with afib and its because the decrease in CO and loss of contraction meds to decreased ventricular filling and so it decreases the preload and leads to severe hypotension and acute pulmonary edema
what are the most commonly occluded coronary vessels
LAD>RCA>circumflex
what is the change in the myocardium after 0-4 hours
no change
what is the change in the myocardium after 4-12 hours
wavy fibers and long myocytes and nuetrophils begin to appear
what is the change in the myocardium after 12-24 hours
myocyte hypereosinophilia with pyknotic nuclei
what are the issues associated with reperfusion
generation of free radicals and leads to hyper contraction of myofibrils through increased Ca influx
what are the major complications in the first 24 hours
entricular arrythmia, HF, cardiogenic shock
what is the change in the myocardium after 1-3 days
extensive coagulative necosis, acute inflammation with neutrophils- lose nuclei and striations
what are the complications in the 1-3 day post MI period
postinfarction fibrinous pericarditis
what is the change in the myocardium after 3-7 days
disintegration of dead neutrophils and myofibers macrophages at the edges
what is the change in the myocardium after7-10 days
robust phagocytosis and granulation tissue
what is the change in the myocardium after 10-14 days
granulation with neovaculature
what are the biggest complications between 3-14 days post MI
free wall rupture leading to tamponade
papillary muscle rupture- mitral regurg holosytolic murmur
interventricular septal rupture due to macrophage mediated structureal degradation
LV pseudoaneursym- risk of rupture creating a VSD
what is the change in the myocardium after 2weeks to months
contracted scar
what are the complications after 2 weeks to several months
dressler syndrome, HF, arryhmias, true ventricular aneurys, with risk of mural thrombis
LAD MI elevations in
V1-V4
RCA MI elevations in
II, III, AVF
LCX MI elevations in
I and AVL
what drugs decrease mortality in HF patients
beta blocker, spiro, and aCE
what is the systolic dysfunction in HF
decreased EF and increased EDV, decreased contratility due to ischemia or dilation of the heart
what is the diastolic dysfunction in HF
decreased compliance, preserved EF< normal EDV but decreased compliance due to hypertrophy
what are the symptoms of let heart fialure
orthopnea, paroxysmal norcutnal dyspnea, pulmonary edema
what are the symptoms of right heart failure
hepatomegalty, jugular venous distnetion, peripheral edema
Giant cell arteritis- what is the histology of the vessel like
intimal thickening, lamina fragmentation and granulomatous nflammation- can read to ophthalmic artery occlusion
Takayasu arteritis
asian females under 40 with pulses upper extremities, fever, night sweats, arthritis, myalgia, skin nodules, ocular disturbance. Granulomatous thickening and narrowing of the aortic arch
what is the determinant of the severity of giant cell arteritis
IL6- the drug is toertizumab for this
if a person has polyarteritis nodosa what might they also have
HBV
what are the symptoms and histology of polyartertitsi nodosa
fever, weight loss, mailase, headache, abdominal pain, melena, hypertension, neurologic dysfunction, cutanoues eruptions, renal damge- usually is transmural inflammation of the arterial wall with fibrinoid necrosis leading to read lmicroaneurysms. It is also immune complex mediated
Kawasaki what is the presentation
asian children under 4 conjunctival injection, rash, adneopathy, strawberry tongue, hand and foot changes, fever- fever is for 5 days
what is the long term complication of Kawasaki and what is the treatment
coronary artery aneursym and aspirin
buerger- presentation and histology- thromboangitis obliterans
heavy smokers, male with intermittent claudication and gangrene and autoamputation of the digits. get segmental thromosing vasculitis it extends to contiguous vessels and nerves
granulomatosis with polyangitis- pathology and what is seen
perforation fo nasal septum, chronic sinusitis, otitis media, mastoidis, hemptypsis, cough, dyspnea, hematuria, red cell casts- focal necrotizing vascultitis, necrotizing granulomas in the lung and upper airway, necrotizing glomerulonephritiss
microscopic polyangitis
ncrotizing vasculitis of the lung, kindy and skin with pouch immune glomerulonepthitis and palpable purport without nasal involvement
eosinophilic granulomatosis with polyangitis
asthma, sinusitis, skin nodules or purport, peripheral neuropathy, heart, GI ,kidneys, pauci immune glomerulonephritis- granulomatous necrotizing vasculitis with eosinophilia- increased IgE
Henoch Schonlein purpura
URI then skin with palpable purport on the legs and butt, arthralgia, abdominal pain, vasculitis from IgA complex deposition. HSN III from deposition of complexes in the small vessels
where is preproinsulin synthesized
rough ER
when is c peptide and insulin increased
sulfonylureas or diabetic drugs that increase the release of insulin or insulinomas
when is insulin and not cpeptide increased
it is when there is an exogenous source of insulin- this can be from factitious disorder or malingering
what does insulin do to target tissues
it brings insulin receptors and it induces glucose uptake into dependent tissues
what kind of activity does insulin receptors have
tyrosine kinase activity
what are the effects of insulin
increased glucose transport to skeletal muscle and adipose tissues, increased glycogen synthesis and storage, increased T G synthesis, increased NA retention, increased cellular uptake of K and amino acids, decreased glucagon, decreased lipolysis
what glucose receptors are on adipose and skeletal muscle
GLUT 4
what glucose receptors are insulin dependent
GLUT 4
what glucose receptors are on RBC, brain, cornea, placenta
GLUT 1
what glucose receptors are on beta cells, liver, kidney, small intestine
GLUT 2
what glucose receptors are on spermatocytes and GI tract and take in fructose
GLUT 5
what glucose receptors are on brain and placenta
GLUT 3
what is the pathway of insulin release from the beta cell
glucose enters the beta cell and it increases ATP which closes the K channels and this depolarizes the membrane allowing for Ca to diffuse across the membrane and this causes the release of insulin by exocytosis
why is there an increased response to glucose if it is oral instead of IV
there are increased incretins if it is given orally which increases the beta cell sensitivity to glucose. Incretins are also called GLP1
what drugs block aromatase
anastrozole, exemestane
what drug blocks five alpha reductasse
finasteride
male has ambiguous genitalia and XX has no secondary sexual dev- increased aldosterone, decreased cortisol, decreased sex hormones, increased BP, and decreased K
17 alpha hydroxylast deficiency
males look normal and have precociuos puberty and females are virilized- decreased aldosterone, decreased cortisol and increased sex hormones, decreased BP, increased BP- increased renin activity, increased 17 hydroxyprogesterone
21- hydroxylase
females are virilized and males look normal- decreased aldosterone but increased 11 deoxycorticosterone so it increased BP, decreased cortisol, increased sex hormones, increased BP, decreased K and decreased renin activity
11 Beta hydroxylase
what is the cheat for CAH
1 in the first digit is HTN and 1 in second digit is virilized
DM type 1 characteristics, genetics, glucose intolerance,
autoimmune destruction of beta cells due to glutamic acid decarboxylase antibodies,always insulin for treatment, under 30 years, no obesity, relatively weak genetics, it is HLA DR3 and 4, and insulin sensitivity, ketoacidosis, Bcells are decreased, decreased insulin levels- classic stmpyoms
what is the histology of DM 1
islet leukocytic infiltrate
DM 2 characteristics, genetics, glucose tolerance
increased insulin resistance, progressive pancreatic beta cell failure, sometimes need unselling, best, very genetic, mild to moderate glucose intolerance, some amyloid deposition i the pancreas,
what is the histology of DM 2
islet amyloid polypeptide- IAPP deposits
the patient is pregnant for 20 days, what should be formed
the neural plate should be formed
when does the notochord and neural development take place
18-20 days
draw circle of willis
are you a winner?
what is the rule of 4’s
4 midline M’s- morot math, medial lemnisucs, MLF, motor CN
4 side S;s- spinocerebella, spinothalamic, sensory V1, sympathetic
4 CN motor are midline and divisible by 12: 3,4,6, 12
what cranial nerves are in the midbrain
3,4
what cranial nerves are in the pons
5,6,7,8
what cranial nerves are in the medulla
9,10,12
what crainal nerve is not in the brianstem
11
contralateral paralysis and sensory loss of the face and upper limb, aphasia if dominant usually the left, and it is the left hemisphere. hemineglect if lesion is nondominat- what vessel is occluded
middle cerebral artery
contralateral paralysis and sensory loss of lower limb cam have some behavioral and urinary incontience- what vessel is occluded
anterior cerebral artery
contralateral paralysis and or sensory loss- face and body. absence of cortical signs like neglect, aphasia, visual field loss- what vessel is occluded
lenticulostriate artery
what does the lenticulostriate artery supply
striatum and internal capsule
what are the common reasons for lenticulostrate artery lesions
lacunar strokes from uncontrolled hypertension
contralateral paralysis of lower limbs, decreased contralateral proprioception, and ipsilateral hypoglossal dysfunction tongue deialtion laterally- what vessel is occluded
anterior spinal artery
medial medullary syndrome
infart of paramedic branches of the asa and or vertebral arteries
vomitting, vertigo, nystagmus, pain and temperature sensation decreased from the ipsilateral face and contralateral body:dysphagia, hoarseness, decreased gag reflex, ipsilateral kroner syndrome ataxia, dysmetria- what vessel is occluded and what is the syndrome called
posterior inferior cerebellar artery- laterally medially syndrome
what area is covered by PICA
it is vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, neucelus ambiguus, sympathetic fibers, inferior cerebellar peduncle
vomiting vertigo nystagmus, paralysis of the face, decreased lacrimation, salivation, decreased taste, ipsilateral pain and temperature of the face and contra of decreased pain and temperature of the body- ataxia and dysmetria– what vessel is occluded
AICA- lateral pons syndrome-facial droop
preserved consciousness, vertical eye moevement, blinking, quadriplegia, loss of voluntary mouth, facial and tongue movement– what vessel is occluded
basilar artery
contralateral hemianopia with macular spearing- contralateral paresthesias, numbness of less and trunk- can’t recognize faces- what vessel is occluded
posterior cerebral artery
Weber syndrome
anterior midbrain infarct from occlusion of the paramedic branches of the posterior cerebral artery- peduncle lesion causes dysphagia, dystonia, dysarthria, contralateral spastic hemiparesis, CN III palsy and eyes are down and out
repetitive brief heaches, excrutiating periorbital pain with lacrimation and rhinorrhea, may present with horner syndrome
cluster headache
what is the treatment for cluster headache
it is sumatriptan and O2 and prophylaxis for verapamil
bilateral- steady pain so photophobia or phonophobia with no aura
tension headache
pulsating pain with nausea, photophobia, phonophobia, aura- due to irritation of CN V, meninges, or blood vessels release of substance P, cancinton gene- related peptide vasoactive peptides
mirgraine
treatment for migraine
NSAID, triptans, dihydroergotamine, beta blocks, ccb, amytripyltine,
dihydroergotamine
induce vasospastic angiana contricts vasuclat smooth muscle and partial agonist for sertonin recptors
positional vertigo
inner ear etiology with semicircular canal debris, vestibular nerve infection, ,inure disease and positional testing- delayed horizonatal nystagmus
what are the symptoms of deniers disease
vertigo, tinnitus, hearing loss- increased pressure and volume of endolymph, recurrent vertigo, ear fullness and pain. unilateral sensineural hearing loss and tints.
central vertigo
brain stem or cerebellar lesion stroke affecting vestibular nuclei or posterior fossa tumor. Directional change of nystagmus, skew deviation, diplopia, dysmetria, positional testing. immediate nystagmus in any direction, focal neurologic
Sturg Wber syndrome
congenital non-inherited somatic developmentally animal of neural crest derivatives due to GNAQ gene. affects small blood vessels and port wine stain in the V1/V2 birth mark. Ipsilateral leptomeningeal angioma with seizures and epilepsy and intellectual disability and episcelral hemangiona- increased intraocular pressure- early onset flaucoma
what is the typical finding of sturg weber
tram track calcifications on opposing dyri
TS findings
hamartomas, angiofibromas, mitral regurgiation, ash lead spots- cardiac rhabdomyosarcoma- rental angiomyolipoma and ungal fibromas
NF1
cade au last spots, litchi nodules- iris hamartomas, cutaneous neurofibromas, optic gliomas, heochromocytoma, mutated NF1, inactivation of RAS on chromosome 17-derived from neural crest cells
VHL
hemangiobalstomas- high vascularity with hyper chromic nuclei and in retina and brain stem, cerebellum, spin, angiomatosis (cavernous hemangioma in skin mucosa and organs), bilateral renal cell carcinoma and pheochromocytoma
osteoporosis what are the lab values
normal lab values
osteopetrosis what are the lab values
decreased Ca
pagets what are the lab values
increased ALP
osteitis fibrous cystica/primary hyperparathyroid what are the lab values
increased CA, decreased phos, increased ALP, increased PTH
secondary hyperparathyroid what are the lab values
decreased CA, increased phos, increased ALP, increased PTH
osteomalacia/rickets what are the lab values
decreased CA, decreased phos, increased ALP, increased PTH
hypervitamin D what are the lab values
increased Ca, increased phos, decreased PTh
pink pearly lesions with telanagtasia and rolled borders with central ulcers and palisading nuceli
basal cell carcinoma
lower lip, hand, ears, local innovation with ulcerative red lesion with frequent scale, adnd chronic draining sinuses has keratin pearls
squamous cell carcinoma
S100 tumor marker and associated wit sunlight and fair skinned persons. depth correlate with mets, ABCS and superficial and depth is associated wit prognsosi
melanoma
neprhotic and nephrtitic syndromes
FA 548
