Blue Flags Flashcards
(346 cards)
1
Q
incidence
A
number of new cases/number of people at risk
2
Q
prevalence
A
number of existing cases/total number of people in pulation
3
Q
what does short disease duration do to incidence and prevalence
A
they should be roughly equal
4
Q
what does long disease duration do to incidence and prevalence
A
prevalence increases over incidence because of the increased number of cases
5
Q
type 1 error
A
false positive
6
Q
type 2 error
A
false negative. related to the statistical power
7
Q
t test
A
checks the difference between 2 means
8
Q
ANOVA
A
checks the differences between the means of 3 or more groups
9
Q
Chi-square
A
checks differences between 2 or more percentages or proportions or categorical outcomes
10
Q
informed consent
A
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
11
Q
patient is non adherent
A
determine reason for non adherence and determine the willingness to change
12
Q
desire unessecary procedure
A
understand why they want the procedure and address underlying concern, Do not reduce or refer to another
13
Q
patient struggles to take medication
A
provide written instructions, attempt to simplify regiments, use teach back method
14
Q
family members ask for information about prognosis
A
avoid discussing issues with relatives without the patients permission
15
Q
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
A
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
16
Q
17 year old girl requests an abortion
A
require parental consent.
17
Q
parents want girl to give up child of 15 yo pre girl
A
girl has rights about the child. discuss options if requested
18
Q
terminally ill patent requests physician assisted suicide
A
refuse involvement of the physician but can prescribe medically appropriate analgesics that coincidentally shorten the patients life
19
Q
patient is suicidal
A
assess the seriousness of the threat suggest the patient remain in the hospital and if not make them stay
20
Q
patient thinks you’re attractive
A
ask direct, close ended questions and use a chaperone. NEVER DATE
21
Q
a woman who had a mastectomy says she now feels ugly
A
find out why the patient feels this way
22
Q
patient is angry about wait time
A
acknowledge the anger and do not take it personally. Do not explain the delay
23
Q
patient is upset with how they were treated by another doctor
A
suggest that the patent speak directly to that physician directly about the concerns
24
Q
an invasive test is performed on the wrong patient
A
inform the patient of the mistake
25
requires a treatment not covered by insarance
never delay or limit care based on this. Discuss all options even if they are not covered
26
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
27
common causes of death by age- under 1
congenital malformations, Preterm birth, SIDS
28
common causes of death- 1-14 years
unintentional injury, cancer, congenital malformation
29
common cause of death 15-34 years
unintentional injury, suicide, homicide
30
common cause of death 35-44
unintentional injury, cancer, heart disease
31
common cause of death 45-64
cancer, heart disease, unintentional injury
32
common cause of death 65+
heart disease, cancer, COPD
33
hospital conditions with high readmission rate- medicare
congesitive HF, septic, pneumonia
34
hospital conditions with high readmission rate- medicaid
mood disorder, schizophrenia, DM
35
hospital conditions with high readmission rate- private insurance
chemo radiation, mood disorder, complications of surgery
36
hospital conditions with high readmission rate- uninsured
mood disorder, alcohol related, DM
37
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
38
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
39
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
40
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.
41
dementia causes- irreversible
AD, Lewy body dementia, HD, Pick, cerebral intact, Mad cow, chronic substance abuse
42
reversible causes of dementia
hypothyroid, dpression ,B12 def, NPH, neurosyphillus, hydrocephalus
43
EEG in delirium vs. dementia
Delirium has a diffuse slowing EEG and dementia has a normal EEG
44
major depression how long before diagnossi
need 2 weeks for symptoms
45
major depression treatment
CBT and SSRI
46
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
47
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
48
dysthymia
persistent depressive disorder- mild depression lasting at least two years
49
atypical depression
mood reactivity- able to cheer up, reversed vegetative, hypersomnia, hyperphageia, leaden paralysis, interpersonal rejection sensitivity
50
Cluster A
paranoid, schizoid, schizotypal
51
pervasive distrust and suscpiciousness; projection is the major defense mechanism
paranoid
52
voluntary withdrawal from social situations, limited emotional expression, content with social isolation
schizoid
53
eccentric appearance, odd beliefs, or magical thinking, awkward in relationships
schizotypal
54
Cluster B
antisocial, borderline, histrionic, narcissitic
55
cluster C
avoidant, OCPD, dependent
56
disregard for and violation of rights or others, criminality, M>F, goes by another name before the age of 18
antisocial
57
unstable mood and interpersonal relationships, impulsive, self-mutiliation, suicidal, sense of emptiness, splitting
borderline
58
excessive emotionality and excitability, attention seeking, sexually provocative, overly concerned with appearance
histrionic
59
grandiose, sense of entitlement, lacks empathy and requires excessive admiration, often demands the best and reacts with rage to criticism
narcissistic
60
hypersensitive to rejection, socially inhibited, timid, feelings of inadequacy, desires relationships with others
avoidant
61
preoccupation with order, perfectionism and control. behavior bothers others but not self
OCPD
62
submissive, clingy, excessive need to be taken care of, exceedingly low self-confidence
dependent
63
Fab region
fragment antigen binding- determines the unique antigen binding pocket only 1 antigen per B cell
64
Fc region
constant region, carboxy terminus, complement binding, carbohydrate side chains
65
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
66
generation of antibody specificity
somatic hypermutation and affinity matuation- variable switching, isotype switching
67
what can antibodies do
prevent bacterial adherence (neutralization), opsonixation (promotion of phagocytosis), complement activation activates C3B and the mac complex
68
what antibody is the most abundant in the serum
IgG
69
what antibody fixes complement, crosses placenta, opsonizes bacteria, and neutralizes bacterial toxins and viruses
IgG
70
what antibody prevent attachment of bacteria and viruses to mucus membrane
IgA
71
what antibody is produced by the GI tract and protects against gut infecttions
IgA
72
what antibody is released into the secretions like tears, saliva, mucus and breast milk
IgA
73
what antibody is the first response to an antigen
IgM
74
what antibody fixes complement but does not cross the placenta
IgM
75
Pentamer antibody
IgM
76
what antibody is found on the surface of B cells
IgD
77
what antibody binds mast cells and basohils
IgE
78
what antibody cross links when exposed to allergen mediating the type I HSN through release of histamine
IgE
79
what antibody mediates defense against worms
IgE
80
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
81
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
82
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
83
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
84
disseminated mycobacterial and fungal infections may present after administration of BCG (Tb vaccine), decreased IFN gamma, decreased Th1 response
IL12 deficiency
85
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
86
noninvasive candida infections of the skin and mucous membranes. Absent invert T cell proliferation response
T cell dysfunction- chronic mucocutaneous candidiasis
87
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
88
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
89
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
90
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
91
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
92
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
93
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
94
deficiency leads to chalices with inflammation of lips scaling and fissures of the corners of the mouth and corneal vascularization-
B2 riboflavin
95
what does B2 do
component for redox reactions
96
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
97
what is Hartnup disease
AR recessive deficiency ot tryptophan and so there is aminoacidura and decreased gut absorption and this means decreased niacin
98
excess of this leads to facial flushing, hyperglycemia and hyperuriciemia
this is niacin
99
what can niacin trat
lower levels of VLDL and raises levels of HDL because its part of NAD and NADP
100
deficiency causes dermatitis, enteritis, alopecia, and adrenal insufficiency
this is from B5 or pantothenic acid
101
deficiency leads to convulstiona, hyper irritability, peripheral neuprpathy, sideroblasts dur to impaired hemoglobin- and causes
B6 deficiency- isoniazid and oral contraceptives
102
function of B6
used for NT
103
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
104
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
105
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
106
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
107
excess is vomiting, nausea, fatigue, calcium oxalate nephrolithiasis, and increased risk of iron toxicity
vitamin C
108
deficiency- rickets ostomalacia, and tetany from the hypocalcemia
D- breastfed do not get it oral low sun exposure, pigmented skin
109
what enzyme activates vitamin D
alpha 1 hydroxylase
110
excess ledas to hypercalcemia, hypercalciuria, loss of appetite, stupor, and grnaulomas
vitamin D
111
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
112
what does vitamin E do
it is an antioxidnat
113
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
114
what does fetus look like with K def
intracranial pressure and refused vaccin
115
deficiency leadsto delayed wound healing, hypogonadism, decreased axillary hair, dysgeusia, anosmia, acrodermatitis enteropathica- why and what
zinc can be from small intestine malabsortion
116
protein malnutrition resulting in skin lesions, and edema from decreased plasma oncotic pressure.
Kwashiorkor
117
total calorie malnutrition resulting in emaciattion like tissue and muscle wasting and loss of subcutaneous fat
marasmus
118
rate limiting enzyme for glycolysis
phosphofructokinase 1
119
rate limiting enzyme for gluconeogenesis
Fructors 1 6 bisphosphate
120
rate limiting enzyme for TCA
isocitrate dehydrogenase
121
rate limiting enzyme for glycogenesis
glycogen synthase
122
rate limiting enzyme for glycogenolysis
glycogen phosphorylase
123
rate limiting enzyme for HMG shunt
G6PD
124
rate limiting enzyme for de novo pyrimidine synthesis
CPS2
125
rate limiting enzyme for de novo purine synthesis
PRPP amidotransferase
126
rate limiting enzyme for urea cycle
CPS1
127
rate limiting enzyme for fatty acid synthesis
acetyl coa carboxylase
128
rate limiting enzyme for fatty acid oxidation
carnithine acyltransferase I
129
rate limiting enzyme for ketogenesis
HMG CoA synthase
130
rate limiting enzyme for cholesterol synthesis
HMG reductase
131
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
132
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
133
derivatives of phenylalanine
tyrosine, thyroxine, dopa, melanine, dopamine, NE, epi
134
derivatives of tryptophan
niacin, serotonin, melatonin
135
derivatives of histidine
histamine
136
derivatives of glycine
porphyrin, heme
137
derivatives of glutamate
GABA and glutathione
138
derivatives of arginine
creatine, urea, nitric oxide
139
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
140
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
141
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
142
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
143
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
144
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
145
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
146
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
147
peripheral neuropathy, developmental delay, optic atrophy, globoid cells and seizures-what is the deficiency, enzyme, and treatment, and what accumulates
Krabbe- galactocerebrosidase
148
central and peripheral demyelination with ataxia and dementia--what is the deficiency, enzyme, and treatment, and what accumulates
Metachromic leukodystrophy- arylsulfatase A
149
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
150
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
151
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
152
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
153
what leads to an increased risk of UTI
vesicoureteral reflux
154
what is there determining risk factor for UTI from cathertization
the duration of catheterization
155
what is the leading cause of UTI
ecoli
156
what is the second leading cause of UTI in sexually active women
staph spare which is novobiocin resistant
157
what is the cause of UTI that has large mucoid capsule and colonies that are viscous
klebsiella
158
what are UTI that have red pigment and drug resistant
serratia
159
UTI with swarming motility and produces urease
proteus
160
UTI with blue green pigment and fruity odor- long term indwelling catheter
pseudomonas
161
no inflammation, but thin white vaginal discharge with dish ordor and clue cells
gardenerlla- treat with metronidazole
162
strawberry cervix, forthy yellow green, foul smelling discharge, motile
trichomonas- metronidazole
163
inflammation with thick white cottage cheese, with pseudohyphae
candida and use azoles
164
congenital infection: bug, and transmission- chorioretinitis, hydrocephalus, and intracranial calcifications and blueberry rash
cat feces, toxoplsmosis
165
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,
166
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
167
congenital infection: bug, and transmission, and mom- recurrent infections, chronic diarrhea
sexual contact or needlestick, low CD4 count, and HIV
168
congenital infection: bug, and transmission, and mom- encephalitis and vesicular lesions
skin mucus membranes, asymptomatic in the mom or some ulcerated lesions HSV 2
169
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
170
STI lesion- painful genital ulcer with exudate and inguinal adenopathy
chancroid- haemophilus ducreyi
171
STI lesion- urethritis, cervicitis, epiddimitis, conjunctivitis, reactive arthritis, PID
chylamydia D-K
172
STI lesion- warts and koilocytes
condylopma accumoinata- HPV
173
STI lesion- painful penile, vulvar, and vercival lesions, ulcers, systemic symptoms such as fever headache, myalgia
HSV2
174
STI lesion- urethritis, PID, prostatitis, epidydimitis, arthritis, creamy purulent discharge
gonorrhea
175
STI lesion- jaundice
HBV
176
STI lesion- infection of lymphatics, painless genital ulcers, painful lymphadenopathy, buboes
lymphogranuloma venereum- C trachomatis L1-L3
177
STI lesion- painless chancre
trponema pallidum- primary syphillus
178
STI lesion- fever, lymphadenopathy, skin rashes, condyloma lata
secondary syphilis
179
STI lesion- gummas, tabes dorsalis, general paresis, aortitis, argyll robertson pupil
tertiary syphilis
180
STI lesion- vaginitis, strawberry cervis, motile on wet prep
trichomonas
181
cervical motion tenderness, purulent discharge, salpingitis, hydrosalpinx, and tubo-ovarian abscess
PID
182
what can happen from PID
ectopic pregnancy, pelvic pain, adhesions
183
what is Fitzhugh Curtis Syndrome
infection of liver capsule and violin string adhesions of peritoneum to liver
184
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.
185
what changes with Michaelis-Menten if there is a competitive inhibitor
It means that the vmax stars the same, but the Kmax is higher,
186
what changes with Michaelis-Menten if there is a non competitive inhibitor
The vmax decreases
187
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
188
In regards to Michaelis-Menten- what is the y axis and x axis
y axis is V and x axis is concentration of substrate
189
In regards to the Lineweaver Burke plot- what happens if the V max decreases
The y intercept is increased as max decreases
190
if there is a reversible competitive inhibitor, what is the effect of Vmax and Km
vmax is unchanged and Km increases
191
If there is a irreversible competitive inhibitor, then there is
a decrease in Vmax and KM is unchanged
192
if there is a noncompetitive inhibitor then there is
a decrease in Vmax and Km is unchanged
193
Which inhibitor can be overcome with increased substrate
the reversible competitive inhibitor can be overcome with substrate
194
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)
195
what happens with oral bioavailability- why does it decrease with oral
High first pass metabolism through the liver leads to decreased serum drug
196
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
197
What is bioavailability of IV
it is 100%
198
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
199
what is the Vd in the blood
low Vd because large charged molecules stay bound
200
what is the Vd in the ECF
it is medium, and small hydrophobic molecules
201
what is the Vd in all tissues including fat
It is high and small lipophilic molecules attached to protein
202
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
203
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
204
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%
205
what is the equation for loading dose
Css x Vd= loading dose
206
what is the equation for maintenance dose
MD= Css x Clearance
207
what does renal and liver disease do to maintenance dose
it decreases the maintenance dose and doesn't change the loading dose
208
what is the additive effect of drug interactions
effect of substance A and B together is equal to the sum of their individual effects
209
what is the permissive effect of drug interactions
presence of substance A is required for the full effects of substance B
210
what is the synergistic effect of drug interactions
effect of substance A and B together is greater than the sum of their individual effects
211
what is the tachyphylactic effect of drug interactions
acute decrease in response to a drug after initial or repeated administration.
212
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
213
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
214
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.
215
what increases SV
increased contractily, increased preload, and decreased after load. a failing heart has decreased SV
216
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.
217
what do venodilators do to preload
decreased preload
218
draw a pressure volume loop and label
yay
219
S1 heart sound
M and T close
220
S2
a p close
221
S3
increased with increased filling pressures like mitral regard or heart failure or dilated ventricles
222
S4
heart as an atrial kick in late diastole from the atria having to contract more forcefully against the hypertrophied ventricles
223
JVP a wave
atrial contraction
224
JVP x wave
atrial relaxation
225
JVP c wave
RV conration
226
JVP v wave
is the RAP increasing from filling
227
JVP y wave
the RV is filling from the RA
228
what does handgrip do to murmurs
it increases the after load which increases mitral regurg, and aortic regard and creates a later MVP click
229
what does valvalva do to murumurs
decreases the preload to it increases hypertrophic cardiomyopathy
230
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
231
crescendo decrescendo murmur systolic- delayed pulses, syncope, angina, dypnea-
AS
232
what is AS usually from
calcification of a bicuspid or normal valve
233
holosystolic hugh blowing murmur
regurg
234
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
235
holosystolic high pitched blowing murmur that is in the right sternal border
causes by RV dilation- TR
236
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
237
holosystolic harsh murmur over the right sternal border
VSD
238
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
239
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
240
continuous machine mumur on S2
PDA can be from congenital rubella and closes with indomethacin and prostaglandin E keeps it open
241
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
242
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
243
what are the most commonly occluded coronary vessels
LAD>RCA>circumflex
244
what is the change in the myocardium after 0-4 hours
no change
245
what is the change in the myocardium after 4-12 hours
wavy fibers and long myocytes and nuetrophils begin to appear
246
what is the change in the myocardium after 12-24 hours
myocyte hypereosinophilia with pyknotic nuclei
247
what are the issues associated with reperfusion
generation of free radicals and leads to hyper contraction of myofibrils through increased Ca influx
248
what are the major complications in the first 24 hours
entricular arrythmia, HF, cardiogenic shock
249
what is the change in the myocardium after 1-3 days
extensive coagulative necosis, acute inflammation with neutrophils- lose nuclei and striations
250
what are the complications in the 1-3 day post MI period
postinfarction fibrinous pericarditis
251
what is the change in the myocardium after 3-7 days
disintegration of dead neutrophils and myofibers macrophages at the edges
252
what is the change in the myocardium after7-10 days
robust phagocytosis and granulation tissue
253
what is the change in the myocardium after 10-14 days
granulation with neovaculature
254
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
255
what is the change in the myocardium after 2weeks to months
contracted scar
256
what are the complications after 2 weeks to several months
dressler syndrome, HF, arryhmias, true ventricular aneurys, with risk of mural thrombis
257
LAD MI elevations in
V1-V4
258
RCA MI elevations in
II, III, AVF
259
LCX MI elevations in
I and AVL
260
what drugs decrease mortality in HF patients
beta blocker, spiro, and aCE
261
what is the systolic dysfunction in HF
decreased EF and increased EDV, decreased contratility due to ischemia or dilation of the heart
262
what is the diastolic dysfunction in HF
decreased compliance, preserved EF< normal EDV but decreased compliance due to hypertrophy
263
what are the symptoms of let heart fialure
orthopnea, paroxysmal norcutnal dyspnea, pulmonary edema
264
what are the symptoms of right heart failure
hepatomegalty, jugular venous distnetion, peripheral edema
265
Giant cell arteritis- what is the histology of the vessel like
intimal thickening, lamina fragmentation and granulomatous nflammation- can read to ophthalmic artery occlusion
266
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
267
what is the determinant of the severity of giant cell arteritis
IL6- the drug is toertizumab for this
268
if a person has polyarteritis nodosa what might they also have
HBV
269
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
270
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
271
what is the long term complication of Kawasaki and what is the treatment
coronary artery aneursym and aspirin
272
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
273
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
274
microscopic polyangitis
ncrotizing vasculitis of the lung, kindy and skin with pouch immune glomerulonepthitis and palpable purport without nasal involvement
275
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
276
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
277
where is preproinsulin synthesized
rough ER
278
when is c peptide and insulin increased
sulfonylureas or diabetic drugs that increase the release of insulin or insulinomas
279
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
280
what does insulin do to target tissues
it brings insulin receptors and it induces glucose uptake into dependent tissues
281
what kind of activity does insulin receptors have
tyrosine kinase activity
282
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
283
what glucose receptors are on adipose and skeletal muscle
GLUT 4
284
what glucose receptors are insulin dependent
GLUT 4
285
what glucose receptors are on RBC, brain, cornea, placenta
GLUT 1
286
what glucose receptors are on beta cells, liver, kidney, small intestine
GLUT 2
287
what glucose receptors are on spermatocytes and GI tract and take in fructose
GLUT 5
288
what glucose receptors are on brain and placenta
GLUT 3
289
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
290
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
291
what drugs block aromatase
anastrozole, exemestane
292
what drug blocks five alpha reductasse
finasteride
293
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
294
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
295
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
296
what is the cheat for CAH
1 in the first digit is HTN and 1 in second digit is virilized
297
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
298
what is the histology of DM 1
islet leukocytic infiltrate
299
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,
300
what is the histology of DM 2
islet amyloid polypeptide- IAPP deposits
301
the patient is pregnant for 20 days, what should be formed
the neural plate should be formed
302
when does the notochord and neural development take place
18-20 days
303
draw circle of willis
are you a winner?
304
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
305
what cranial nerves are in the midbrain
3,4
306
what cranial nerves are in the pons
5,6,7,8
307
what cranial nerves are in the medulla
9,10,12
308
what crainal nerve is not in the brianstem
11
309
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
310
contralateral paralysis and sensory loss of lower limb cam have some behavioral and urinary incontience- what vessel is occluded
anterior cerebral artery
311
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
312
what does the lenticulostriate artery supply
striatum and internal capsule
313
what are the common reasons for lenticulostrate artery lesions
lacunar strokes from uncontrolled hypertension
314
contralateral paralysis of lower limbs, decreased contralateral proprioception, and ipsilateral hypoglossal dysfunction tongue deialtion laterally- what vessel is occluded
anterior spinal artery
315
medial medullary syndrome
infart of paramedic branches of the asa and or vertebral arteries
316
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
317
what area is covered by PICA
it is vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, neucelus ambiguus, sympathetic fibers, inferior cerebellar peduncle
318
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
319
preserved consciousness, vertical eye moevement, blinking, quadriplegia, loss of voluntary mouth, facial and tongue movement-- what vessel is occluded
basilar artery
320
contralateral hemianopia with macular spearing- contralateral paresthesias, numbness of less and trunk- can't recognize faces- what vessel is occluded
posterior cerebral artery
321
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
322
repetitive brief heaches, excrutiating periorbital pain with lacrimation and rhinorrhea, may present with horner syndrome
cluster headache
323
what is the treatment for cluster headache
it is sumatriptan and O2 and prophylaxis for verapamil
324
bilateral- steady pain so photophobia or phonophobia with no aura
tension headache
325
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
326
treatment for migraine
NSAID, triptans, dihydroergotamine, beta blocks, ccb, amytripyltine,
327
dihydroergotamine
induce vasospastic angiana contricts vasuclat smooth muscle and partial agonist for sertonin recptors
328
positional vertigo
inner ear etiology with semicircular canal debris, vestibular nerve infection, ,inure disease and positional testing- delayed horizonatal nystagmus
329
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.
330
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
331
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
332
what is the typical finding of sturg weber
tram track calcifications on opposing dyri
333
TS findings
hamartomas, angiofibromas, mitral regurgiation, ash lead spots- cardiac rhabdomyosarcoma- rental angiomyolipoma and ungal fibromas
334
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
335
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
336
osteoporosis what are the lab values
normal lab values
337
osteopetrosis what are the lab values
decreased Ca
338
pagets what are the lab values
increased ALP
339
osteitis fibrous cystica/primary hyperparathyroid what are the lab values
increased CA, decreased phos, increased ALP, increased PTH
340
secondary hyperparathyroid what are the lab values
decreased CA, increased phos, increased ALP, increased PTH
341
osteomalacia/rickets what are the lab values
decreased CA, decreased phos, increased ALP, increased PTH
342
hypervitamin D what are the lab values
increased Ca, increased phos, decreased PTh
343
pink pearly lesions with telanagtasia and rolled borders with central ulcers and palisading nuceli
basal cell carcinoma
344
lower lip, hand, ears, local innovation with ulcerative red lesion with frequent scale, adnd chronic draining sinuses has keratin pearls
squamous cell carcinoma
345
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
346
neprhotic and nephrtitic syndromes
FA 548
