test #32 4.22 Flashcards
note, first question on EBV in test #31 accidentaly
when is hCG detectable
secreted by syncitiotrophoblasts.
zygote implants as blastocoele ~8 days
when does zygote enter uterus
zygote enters uterus as 2-8 celled embryo / morula on day 3-4
hCG production by embryo/zygote begins? in maternal serum
free-floating blastocyst in uterine secretes hCG ~6 days, but won’t enter maternal serum until implanatation.
no early than 6-11 days post ovulation in maternal serum (usu day 8)
CMV retinitis
inflammatory vascular sheathing & hemorrhage
full thickness retinal necrosis & edema. eventually replaced w/ atrophic scar
can result in retinal detachment – tearing of thin atrophic scar that forms in areas of prior inflammation
when does CMV infect HIV+ patients?
CD4 < 50 cells/uL
flucytosine mechanism
converted to 5-FU by fungal cytosine deaminase.
causes RNA miscoding and inhibtion of DNA synthesis
IFN-alpha used to treat (4)
(1) hep B and C
(2) hairy cell leukemia
(3) condyloma acuminatum
(4) Kaposi sarcoma
pentamadine rx for?
pneumocystis pneumonia
friedrich ataxia inheritence
autosomal recessive
pathogenesis in friedrich ataxia? presentation
(1) posterior column and spinocerebellar tract degeneration
(2) loss of larger sensory cells of dorsal root ganglion
children 5-15 y/o w/ gait ataxia (wide-based gait w/ difficulty maintaining balance, progressively slow and clumsy
5 symptoms associated w/ friedrich’s ataxia
- progressive ataxia of all 4 limbs, cerebellar dyfxn, early. degeneration of dorsal column – loss of position and vibration
- hypertrophic cardiomyopathy in more than 50% of patients –> cardiac arrhythmia and CHF
- skeletal abnormalities: kyphoscoliosis, pes cavus, hamemrtoes
- diabetes mellitus in about 10%
most common cause of death in friedrich’s ataxia? (2)
cardiomyopathy
bulbar dysfxn (unable to protect airway)
trinucleotide repeat of friedrich’s ataxia. chromosome? codes for?
autosomal recessive
chr. 9
GAA
codes for frataxin = iron binding protein
mitochondrial dysfunction
eroded teeth enamel and enlarged, firm parotid glands, irregular menses (not amenorrhea though)
bullimia nervosa
amenorrhea = almost always in anorexia nervosa
glucagon’s action in DKA
(1) stimulate ketoacid synthesis in adipose tissue
(2) increases glyocogenolysis
(2) gluconeongeisis
(4) lipolysis
(5) urea production
JVP waves
peak: A peak : C dip: x peak: V dip: y
a: atrial contraction
c: bulging of tricuspid valve into atrium (isovol contraction)
x: opening of pulmonic valve / relaxation of atrial muscle
v: continuous flow of venous blood into atria
y: opening of tricuspid valve (passing emptying)
sign of contrictive pericarditis on JVP wave
y descent is deeper and steeper on inspiration
causes of (chronic) constrictive pericarditis
go from 1-3mm to 4-20mm thick. looks like thick line surrounded heart
caused by radiation therapy to chest, cardiac surgery, and TB
evidence of ischemic heart disease on CT?
calcified vessels
clinical signs of constrictive pericarditis
slowed progressive dyspnea, peripheral edema, ascites
what provides nerves, arteries, veins, and lymphatics to ovaries
suspensory ligament
broad ligament
mesoovarium that covers ovaries, uterine tube, ovarian ligament, round ligament of uterus, portion of suspensory ligament.
blood supply and drainage of ovaries
gonads!
blood supply from aorta.
right drains to IVC
left to renal vein
nervous supply to ovaries
from vagus n.
common complication in pelvic surgery when ligating ovarian vessels
ligating ureter (traveling underneath)
round ligament of uterus
courses through inguinal canal. links uterus to external genitalia. contains artery of sampson, which is rarely a source of blood.
also round ligament in liver
ovarian ligament
contains no vessels. courses form uterine pole of ovary to body of uterus, just below uterus
transverse cervical ligament, or cardinal ligament
extends from cervix and lateral fornix of vagina to lateral pelvic walls.
contains uterine artery!
gingival bleeding, echymoses & petechiae, impaired wound healing. perifollicular hemorrhages w/ coiled (corkscrew hairs)
collagen problem.
scurvy: lysyl hydroxylase and proyl hydroxylase deficiency
requires vitamin C
occurs in rough ER
mutation:
- decreases amount of collagen secreted
- impairs triple helix stability
- impairs covalent cross link formation
collagen mutation in ehlers-danlos (type I & II)
mutation in type V collagen
defining characterestics of ehlers-danlos type I & II
joint hypermobility
hyperextensible, fragile, skin
osteogenesis imperfecta mutation
type I collagen.
spontaneous fracture, bone & tooth malformation, blue sclerae
how does dopamine come to inhibit prolactin secretion in pituitary
via tuberoinfundibular dopaminergic pathway – connect hypothalamus to pituitary gland
mucicarmine stain
cryptococcus neoformans. detects polysaccharide capsule
(only one w/ capsule)
round yeast cells w/ narrow-based buds
(can cause pulmonary infxn first)
blastomyces dermatididis on culture
lung & disseminated.
round yeast
broad-based budding
thick, doubly-reflective wall
histoplasma on culture
TB pulmonary & disseminated
intracellularly within macrophages – small, ovoid, budding yeast cells
coccidioides immitis
lung in competent.
disseminated in compromised.
large, irregularly sized, thick walled spherules w/ small, round endospores
only pathogenic fungus w/ polysacch capsule?
cryptococcus neoformans!
red on mucicarmine stain.
clear in india ink.
cystic degeneration of the putamen
many can cause. usmle = think wilson’s disease
sudden cardiac death in youth? in adults?
youth: Vfib from hypertrophic cardiomyopathy
adult: 80% due to acute plaque change superimposed on coronaryatherosclerosis
90% of cardiomyopathies are..
dilated cardiomyopathy! but only account for 10-15% of sudden cardiac death
why do babies need brown fat (5% of their body mass)
susceptible to hypothermia:
- immature nervous system
- high body surface are to volume ratio
- decreased ability to shiver for heat production
white vs brown fat.
white: one intracytoplasmic fat droplet
brown:
- several fat vacuoles,
- considerably more MITO (colour)
- higher oxygen requirement
- contains more capillaries
how does brown fat make heat
uncouple electron transport and phosphorylation.
protons pumped out why electron transport chain return to matrix via mitochondrial matrix protein THERMOGENIN (uncoupler).
no ATP synthesizes, energy = heat
ascending paralysis post febrile illness
guillian barre
guillan barre is associated w/
young adults.
preceeded by upper respiratory or GI infection. could be after vaccine or allergic reaction.
strongly associated w/ campylobacter jejuni infection
pathogenesis of guillan barre
ACUTE DEMYELINATING DISEASE. immune-mediated.
antibodies to infection cross-react w/ myelin of spinal roots & peripheral nerves.
light microscopy of guillan barre
segmental demyelination of peripheral nerves. accompanied by endoneural inflammatory infiltrate – lymphocyte & macriohages
endoneural inflammatory infiltrate =
guillan barre
CSF in guillan barre:
increase protein, with normal/slightly elevated cell count
= ALBUMINOCYTOLOGIC DISSOCIATION
polymyositis vs. guillan barre?
nerves are fine in polymyositis, despite weakness.
guillan barre – NO DTRs
flat yellow spots on inner surface of aorta
fatty streaks
fate of fatty streaks
earliest lesions in progression to atherosclerosis, BUT do NOT predict occurance or location of atheromatous plaques later in live.
in all individuals after age 10
often occur in regions not particularly prone to atheroma. frequently affect people/regions w/ low lifetime incidence of atheromatous plaques
what are fatty streaks
intimal lipid-filled foam cells.
derivived from macrophage and smooth muscle cells that have engulfed LDL, entered intima through injured, leaky endothelium.
usu begin as multiple yellow spots (1mm in diameter) which form streaks.
NOT raised, so do NOT disturb blood flow.
NOT ALL PROGRESS to atheromas! common age 10 onwards. mostly consist of macrophages.
nitric oxide originates from
amino acid arginine
urea originates from..
arginine + aspartate
heme originates from
succinyl-CoA and glycine
creatine originates from
glycine + arginine + SAM
GABA originates from
glutamate
glutathione originates from
glutamate
pyrimidines originate from..
glutamate + aspartate
purines originate from..
glutamate + aspartate + glycine
histidine originates from…
histamine
dopamine pathway origination
phenylalanine -> tyrosine -> DOPA -> dopamine
tryptophan makes.. (2)
tryptophan -> serotonin -> melatonin
&
tryptophan -> niacin
tyrosine makes (2)
thryoxine & melanin
which factors stimulate vasodilation of epicardial vessels?
acetylcholine, bradykinin, shear stress, serotonin, substance P.
all stimulates influx of Ca2+ in endothelium. turns on eNOS
eNOS:
arginine+ O2 -> nitric oxide + citrulline
NO from endothlium goes to smooth muscle cells in vasculature –> turns on guanylate cyclase to make cGMP – vasodilates
cGMP causes vasodilatoin bc protein kinase G reduces cytosolic calcium levels
amino acid w/ adjunctive role in rx of conditions that improve w/ vasodilation
arginine! precursor to nitric oxide
location of enhancers? promoters?
enhancers: increase rate of transcription intiation through protein binding & intxn w/ transcription factors bound to promoter sequences.
enhancer/repressors: anywhere: upstream. downstream, in gene, thousands bp away, sep chromosomes
promoter: binding site for transcription factor and RNA pol II.
two types of promoter:
- TATA (hogness) box: 25 nucleotides upstream from gene
- CAAT box, 70-80 bases upstream from gene
tetanus route
clostridium tetani spores germinate in wound (low oxygen, high nutrients). u
pon bacterial cell autolysis, TOXIN is released and enters motor neuron (axon terminal).
TOXIN travels via retrograde transport to spinal cord, medulla.
ORGANISM stays at site of wound
route of rabies virus
wound -> neuron axons -> salivary glands.
specifically: motor neuron -> retrograde into nerves of spinal cord -> into cerebellum, brainstem -> hippocampus.
from there -> within nerve axons –> tissue of salivary glands
route of diptheria toxin
fibrinous exudate (pseudomembranous exudate) -> blood stream systemic circulation -> cortical neurons & cardiac cells
pressure volume curve of lung & chest wall compliance.
alveolar transmural pressure
chest wall transmural pressure
intrapleural pressure?
lung transmural pressure: ALWAYS + (wants to collapse)
chest wall:
usually - (wants to expand,
except at maximal inspiration, will be +
when positive alveolar transmural pressure = negative chest wall transmural pressure –> airway pressure = 0 (functional residual capacity)
intrapleural pressure: always negative. at FRC (-5cmH20). in inspiration (-7.5cmH20) –> helps draw air into lungs
explain why intrapleural pressure is always negative (even at 0 airway pressure)
recall: pneumothorax, make intrapleural pressure = 0 (atmospheric pressure)
this causes lung to collapse and chest wall to expand.
at FRC –> tendency of chest wall to expand and lung to collapse creates a negative intrapleural pressure of -5cm H20 (more negative when inspire)
rx for amiodarone-induced hypothyroidism?
levothyroxine. typically continue.
always monitor TSH before giving amiodarone
HIV associated esophagitis (3). distinguish?
cannot distinguish clinically. endoscopic & microscopic
(1) candida albicans
- patches of adherent, grey/white pseudomembranes on erythematous mucosa
yeast cells and pseudohyphae invade mucosal cells
(2) Herpes simplex
- small vesicles that evolve into typical “PUNCHED out” ulcers
eosinophilic intranuclear inclusions (cowdry type A) in multinuclear squamous cells at margins of ulcer
(3) CMV
- LINEAR ulceration
both intranuclear and cytoplasmic inclusions
babesia infection
tick bite. endemic in northeast US.
influenza-like symptoms, hepatosplenomegaly, anemia.
often in asplenic patients
isospora belli
profuse, watery diarrhea in HIV patients.
also cryptosporidium spp.
chronic trypanosoma cruzi infection
Chagas disease.
dilated cardiomyopathy, achalasia & megaesophagus, megaolon, megaureter
esophageal involvement of scleroderma (2)
- abnormal peristalsis (dysphagia)
2. lower LES tone (GERD)
janeway lesions: painful or not?
osler nodes: painful or not?
janeway: NOT PAINFUL
osler: PAINFUL. osler = ouch!
janeway lesions
small erythematous, possibly hemorrhagic macules that appear on soles of feet and palms in pt w. bacterial endocarditis.
caused by septic microemboli to cutaneous vasculature.
emboli = infected intracardiac vegetations (bacteria, neutrophil, necrotic materia)
osler nodes
painful papulopustules on pulps of fingers and toes.
cycloserine
inhibits incorporation of D-alanine into UDP-MUrNAc-oligopeptide during bacterial cell wall synthesis.
HIGH level of ototoxicity, rarely used
polymixin
binds to, disrupts, and interferes w/ permeability of cytoplasmic membrane
cysteinuria
autosomal recessive. only issue is stones
defective PCT and intestinal (jejunal) reabsorption of dibasic amino acid.
cysteine, ornithine, lysine, and arginine.
risk for cysteine stones –> hexagonal.
diphenhydramine on sleep
H1 receptor inhibitor.
reduce time to sleep onset & increase depth of sleep.
benzodiazepine 3 effects
- anxiolytic
- muscle relaxant
- anticonvulsant
dystonia
neurological movt disorder
sustained involuntary muscle contractions. force certain parts of body into abnormal, painful movements or postures.
may affect single muscle or group.
(i.e. writer’s cramp, spasmodic torticollis, blepharospasm)
spasmodic torticollis
cervical dystonia. most common focal dystonia
blepharospasm
second most common focal dystonia.
involuntary, forcible closure of eyelids.
initial symptom is uncontrollable blinding.
later -> complete closure of eyelids
myoclonus
sudden, brief, severe muscle contraction
physiologic myoclonus
hiccups and hypnic jerks (occurs when falling asleep)
chorea
involuntary muscle activity that flows from one muscle group to another. may appear fragmented or jerky. may display dancing gait.
hemiballism
flinging of limbs on one side of body. due to contralateral injury of STN.
essential tremor (postural) vs. resting tremor vs. intention tremor
essential: action, exacerbated by holding position (genetic predisposition)
resting: uncontrolled movement, alleviated by intentional movement (parkinsons)
intention: zig-zag motion when pointing/extending to target (cerebellar dysfunction)
rx for essential tremor
b-blocker and primadone (anticonvulsant that becomes phenobarb and PEMA)
progressive EKG findings of acute MI
- peaked T waves –> local hyperkalemia
- ST-segment elevation (min-hrs)
- Q waves (hr-days)
transmural infarct usu caused by..
acute plaque change (rupture) w/ superimposed thrombus that completely occludes involved coronary artery
stable angina begins w/ how much occlusion
75% occlusion
ulcerated atherosclerotic plaque w/ partially obstructive thrombus
unstable angina, subendocardial MI, sudden cardiac death
rx for early ectopic pregnancy (<6 wks)
methotrexate, will accumulate in rapidly dividing trophoblasts
THF is important for what 3 general processes
- thymidine synthesis (DNA)
- amino acid synth
- purine synthesis
folinic acid is..
N5-formyl-THF
N5-N10 methyelene THF
DHF is important for which 2 rxns?
folic acid -> DHF
DHF -> THF
mechanism of methotrexate
structually similar to folic acid. enters cell, converted to polyglutamate form.
polyglutamate form prevents movt of MTX out of cell.
(folate & DHF are stored in cells this way too)
how is folate and DHF stored in cells?
polyglutamation
PABA
folic acid precursor in prokaryotes. sulfonamide antibiotics are chemical analogues.
humans can’t convert PABA into folic acid. so we gotta eat folate
folinic acid (leucovorin)
pre-reduced form of folic acid that can be used for synthesis of purine & thymidylate without first being converted by DHF reductase.
rescue therapy w/ MTX
hep B mediated HCC?
hep C mediated HCC?
hep B: integration into host genome: -inflammation -HBx protein disrupts hepatic cell growth & -blocks p53
hep C:
does NOT integrate
- chronic inflammation etc.
familial hypercholesterolemia
autosomal DOMINANT mutation in LDL receptor
- can’t take up LDL into liver.
serotonin syndrome drugs
sinners ONLY sell LACED drugs that truly make me trip &&..
TRAMADOL, ONDANSETRON (5-HT3 antagonist), LINEZOLID
st. john's wort ondasetron selective 5-HT reuptake (inhibitors (SSRI & SNRI) linezolid dextromethorphan TCA tramadol MAOi meperidine triptans
serotonin syndrome presentation (3)
(1) neuromuscular excitation: hyperreflexia, clonus, myoclonus, rigidity
(2) autonomic stimulation: hyperthermia, tachycardia, diaphoresis, tremor
(3) altered mental status: agitation & confusion
rx for serotonin syndrome
cryptoheptadine 5-HT2 receptor antagonist
linezolid
serious gram positive infections (VRE and MRSA). weak monoamine oxidase inhibitor. can ppt serotonin syndrome
doxycycline toxicity
photosensitivty, pill induced esophagitis.
enamel hypoplasia or permanent tooth discoloration
which commonly used drugs can ppt serotonin syndrome in a patient using SSRIs etc?
tramadol, ondansterone, and linezolid
propanonol helps hyperthyroidism by.. (2)
(1) reduce symptoms (thyroid hormone upregulate b-adrenergic expression)
(2) reduce peripheral conversion of T4 to T3
3 drugs that block peripheral conversion of T4 -> T3?
(1) PTU
(2) ipodate
(3) b-blockers
which hormone upregulates beta-receptor expression? alpha-receptor?
beta-receptor: thyroid hormone (increase HR, anxiety)
alpha-receptor: cortisol (increase BP)
which hyperthyroid symptoms are NOT improved by beta-blockers?
- increased tissue oxygen consumption
- circulating thyroxine levels
- weight loss
- exopthalmosis (graves)
helps w/ HR and anxiety!
crystals in gout?
monosodium uraate
where can monosodium urate crystals deposit?
(1) joint
(2) tissue -> tophi nodules
describe gouty arthritis
monosodium urate ppts in joint, eaten by neutrophils –> inflammatory response
typical gout patient and presentation
- 40-60 y/o obese patient.
- MONOarticular (podagra, usu MTP)
- acute onset joint pain, warmth, erythema, swelling
will resolve w/o treatment
definitive diagnosis of gout?
synovial fluid analysis: increased WBC, mostly NEUTROPHILS.
micropscoy: monosodium urate crystals: parallel -> yellow, negatively birefrigent under polarized light.
negative birefringence means..
aligned parallel to ray -> yellow
aligned perpendicular -> blue
uric acid into joint?
does NOT cause gout. need monosodium urate crystals, not just uric acid.
pseudogout?
clinically just like gout.
joint: see rhomboid blue crystals of calcium pyrrophosphate.
affects both genders. larger joints.
calcific tendonitis
deposits of calcium hydroxyapatite crystals in periarticular soft tissue (esp tendon)
usu rotator cuff
what deposits in joints during gout?
monosodium urate.
NOT uric acid.
organs primarily affected in hemochromatosis (4)
liver, heart, and pancreas
& skin
hemachromatosis inheritance
autosomal recessive
budd-chiari
syndrome secondary to thrombotic occlusion of hepatic vein OR intra/suprahepatic IVC
increased sinusoidal pressure –> portal HTN, ascites, hepatomegaly, splenomegaly
patient younger than 30 y/o with unexplained chronic hepatitis?
consider WILSON’s disease.
low ceruloplasmin, increase urinary Cu2+ excretion, Kayser-Fleischer rings
rapid correction of hyponatremia can cause..
low to high, pons will die
osmotic demyelination.
central pontine myelinolysis
locked-in syndrome:
- spastic quadriplegia: demyelination of corticospinal tracts
- pseudobulbar palsy: demyelination of corticobulbar tracts of CN IX, X and XI
pseudobulbar palsy is..
bulbar palsy?
head & neck muscle weakness, dysphagia, dysarthria.
pseudobulbar = NUCLEI of corresponding cranial n. IN TACT.
bulbar palsy = pathologic process in nuclei of these tracts
rapid correction of hypernatremia can cause
cerebral edema
magnesium citrate & polyethylene glycol are..
osmotic laxatives – distend intestinal wall and increase peristalisis
rectal prolapse
protrustion of rectal mucosa through anus
associated w/ pregnancy & constipation & severe diarrhea & cystic fibrosis
composition of keratin (3)
(1) alanine & (2) glycine
small, tightly coil, many H bonds
& (3) cysteine
disulfide allows for rigidity
vimentin is a marker for
mesenchymal cells – intermediate filament
RNA pol I makes
18S, 5.8S, 28S rRNA
(from single: 45S pre-RNA gene that is then cleaved)
only in nucleolus
RNA pol II makes (3)
- mRNA
- snRNA (small nuclear: mRNA splicing and transcription regulatoin
- miRNA (micro: silencing via translation arrest / mRNA degradation
RNA pol III makes (2)
- tRNA
2. 5S rRNA (essential component of 60s ribosomal subunit)
production of rRNA
45s pre-rRNA genes divided among multiple chromosomes.
arranged into clusters called “nucleolar organizing regions” –> such that all copies are located in nucleolus
role of nucleolus
- transcribe rRNA
- maturation & assembly of ribosomal subunits
(ribosomal protein componenets are made in cytoplasm and brought into nucleolus).
complete ribosome is shuttled out of nucleus.
5s rRNA is special bc
only rRNA located outside of nucleolus (made by RNA Pol III)
classic signs of mononucleosis
sore throat
moderate - high fever
cervical lymphadenopathy
splenomegaly
h. pylori associated w/ what malignancies
gastric adenocarcinoma
MALToma
