UW Deck 2 Flashcards
runs through ventral pons
fibers of CNs 5-8, corticospinal tracts, medial lemniscus, lateral spinalothalamic tract
vagus by the ear
auricular branch: cutaneous sensation of posterior external auditory canal; stimulation of vagal nerve with otoscope speculum –> decrease HR and BP –> vasovagal syncope event
sensation to most of external auditory canal
trigeminal nerve
facial nerve PANS efferent
salivation: submandibular and sublingual
viral myocarditis histology
lymphocyte infiltrate, focal necrosis
heart failure + recent viral infxn
dilated cardiomyopathy due to viral myocarditis (virus damages heart) –> systolic dysfunction
LVH, concentric hypertrophy
diastolic dysfunction –> wall stress –> heart failure/systolic dysfunction
dilated cardiomyopathy
dx of exclusion (pericardial dz, CAD, valvular dz, congenital dz, cardiac rhythm disturbances), systolic dysfunction, decreased stroke volumes, increased end volumes, regurgitation, dilation of all 4 chambers, primary (idiopathic), secondary (exogenous toxic agents)
vasopressin increases reabsorption of
water and urea @ inner medullary collecting duct, V2-receptor mediated
kidney filtration
simple diffusion depending on starling forces; filtration coefficient (kf) depends on area of capillary available for diffusion and permeability of capillary membrane; net filtration pressure (use oncotic and hydrostatic pressure – don’t need coefficient)
calcium handling in kidney
50-60% filtered ca reabsorbed in proximal tubules (paracellular pathway), reabsorption by distal tubule depends on parathyroid hormone
creatinine
freely filtered, secreted a litle by proximal tubules
PAH
freely filtered, entirely secreted by proximal tubules
wolff-parkinson-white
accessory AV conduction pathway: conduction reaches ventricles via accessory pathway slightly faster than AV nodal pathway –> recurrent paroxysmal supraventricular tachycardia, ventricular preexcitation, shortened PR interval, delta wave at start of QRS, widened QRS. Can also set up reentry arrhythmia (down AV node, up accessory pathway, normal QRS)
ST segment
plateau phase
T wave
ventricular repolarization
viral meningitis (vs. bacterial)
lymphocytic predominance, slightly elevated CSF protein, no organism on CSF gram stain and culture, more moderate symptoms (no stupor, coma, severe meningeal irritation)
bacterial meningitis (vs. viral)
high protein, low glucose, neutrophils predominate, really high WBC, often positive CSF culture/gram stain; mental status changes, seizures
meningitis common sx
fever, headache, nuchal rigidity, photophobia, painful extraocular movements
aseptic meningitis bugs
MCC: enterovirus family: coxsachie, poliovirus, echovirus, enterovirus; enterovirus = fecal-oral transmission, don’t cause gastroenteritis
adult bacterial meningitis bugs
- s pneumo, 2. n meningitis
polio virus
fever, malaise, aseptic meningitis –> myalgia, asymmetric paralysis (legs), damages anterior horn LMN –> hyporeflexic
aseptic meningitis via respiratory droplets
varicella, mumps, adenovirus, these 3 can also cause encephalitis
sexually transmitted viruses that can cause aseptic meningitis
HIV and HSV 2 more common than HSV 1, EBV, and CMV
arboviruses that can cause aseptic meningitis
togaviridae, flaviviridae, bunyaviridae; most common in summer and fall when arthropods are most active
meningitis in HIV/AIDS
cryptococcus neoformans
cryptococcal meningitis
headache/fever/lethargy, immune compromised (cancers), low glucose, increased protein, lymphocytes predominate, increased cell count; transparent capsule on india ink stain of CSF (ink stains background, bug stays transparent), thick polysaccharide capsule
listeria meningitis
ampicillin, GP rod, tumbling motility
fungal cell wall
not made of peptidoglycan
increased mixed venous blood oxygen
abnormal hb (binds with greater affinity to oxygen), oxidative metabolism inhibition (cyanide toxicity)
Obstructive lung disease
increase PaCO2
Diffusion problem
calculate A-a gradient; more normal PaCO2 (because it diffuses 20x better than oxygen) decreased PaO2
Perfusion problem
CO2 and O2 do not equilibrate with outside
Calculate A-a gradient
arterial PO2 given by ABG; PAO2 @ sea level (alveolar gas equation) = 150 - (PaCO2/0.8)
normal A-a gradient
10-15 mmhg
normal PAO2 –> normal PaO2
104 mmhg –> 95-100 mmhg (below 95: hypoxemia); drop occurs due to bronchial venous blood
PO2
inspired air: 160 mmhg –> mixes with water in trachea: becomes 150 mmhg –> alveolus: 104 mmhg; venous blood equilibrates with alveoli (40 mmhg –> 104 mmhg) –> drops to 95-100 mmhg because of bronchial venous blood
PCO2
venous blood PCO2: 45 –> alveolar PCO2 = 40 –> trachea CO2: 0 mmHg
venous/alveolar equilibration
NL: full equilibration after passing through 1/3 of capillaries (fast diffusion, perfusion-limited equilibration); if capillary perfusion is poor: slower or incomplete equilibration; tracheal air = alveolar air; venous blood = arterial blood
poor ventilation, what would alveolar gas composition be?
close to venous gas composition
diffusion-limited gas exchange
emphysema, pulmonary fibrosis, exercise (high perfusion)
4 major causes of hypoxemia
right to left shunt (congenital heart diseases); V/Q mismatch (pneumonia, COPD, pulmonary embolism); alveolar hypoventilation (sedative overdose, sleep apnea, myasthenia gravis, high altitude –> low oxygen pressure in alveoli); diffusion problems (alveolar hyaline membrane disease)
cryptococcus neoformans
immunocompromised patients, inhaled –> asx lung infection/pulmonary cryptococcosis (mucicarmine stain lung tissue and bronchoalveolar washings) –> meningitis (india ink CSF); serologic testing (latex agglutination) to detect capsular antigen in CSF
oral thrush
white plaques, associated with immunosuppression, diabetes, antibiotics, steroids\
esophagitis
HIV+ candida infection, odynophagia, dx with endoscopy + bx
renal osteodystrophy
decreased calcitriol (active vitamin D), retention of phosphates (bind Ca –> exacerbates hypocalcemia) –> hyperparathyroidism + more bone turnover (exacerbates hyperphosphatemia)
hypercoagulable state
surgery
marantic endocarditis
disseminated cancer associated with hypercoagulability –> NBTE (non-bacterial thrombotic endocarditis)
non-bacterial thrombotic endocarditis (NBTE)
sterile fibrinous vegetations along edges of valves = thrombus, no inflammation, often due to hypercoagulable state due to underlying disease
trousseau’s sign
tumor-associated procoagulants release –> migratory thrombophlebitis (seen in pts with disseminated cancers)
hypercalcemia in hospitalized pt
hypercalcemia of malignancy, pth-like substance from tumor
extrahepatic biliary atresia
congenital, jaundice, dark urine/light stools, conjugated hyperbilirubinemia, intrahepatic bile ductular proliferation, portral tract edema and fibrosis, parenchymal cholestasis, increased alk phos, ggt
hemolytic disease in Rh+ newborn
jaundice, unconjugated hyperbilirubinemia, hemolytic anemia, + coombs test
gilbert dz
mild unconjugated hyperbilirubinemia during stress
A1AT deficiency, effect on liver
hepatic intracytoplasmic inclusions that are eosinophilic on H&E, strongly PAS positive
physiologic jaundice
goes away after a week
d-isoimmunization
Rh disease
most potent chemotactic eicosanoid
leukotriene B4 (also 5-HETE = leukotriene precursor)
irreversible changes in ASD
chronic pulmonary HTN –> permanent eisenmanger syndrome, pulmonary sclerosis so severe/irreversible that you can’t fix the ASD because the RV won’t be able to pump; atrial and ventricular enlargement can be reversed
long qt syndrome
if pt is otherwise healthy, long qt = congenital issue, predispose to torsades to points –> syncope or death; 2 common congenital disorders related to K+ channel mutation –> delayed rectifying K+ current
jervell and lange-nielsen
autosomal recessive, neurosensory deafness, long qts
romano-ward syndrome
more common than jervell and lange-nielsen, no deafness, long qt
sudden onset syncope
suggests arrhythmia
qt
start of qrs –> up to t wave
mutations that cause dilated cardiomyopathy
mutations that affect cytoskeleton proteins or mitochondrial enzymes
HOCM
syncope upon exertion
sarcoidosis
immune mediated = disordered immune regulation –> intraalveolar and interstitial accumulation of CD4 T cells –> high CD4/CD8 ratio in bronchoalveolar lavage fluid (differentiates sarcoidosis from hypersensitivity pneumonitis or AIDS-related lymphocytic interstitial pneumonitis - have low CD4/CD8 ratios)
high neutrophils in lungs
bacterial PNA, acute toxic injury
high CD8 cells in lungs
lung transplant + chronic rejection
intussusception
impaired venous drainage, necrosis, colicky abdominal pain, current jelly stools = mucus + blood
inferior mesenteric vein
does not course with the inferior mesenteric artery, drains into splenic vein –> portal vein
celiac trunk
supplies foregut except mouth, pharynx, proximal esophagus
internal iliac supplies certain parts of the gut
middle rectal artery, inferior rectal artery (via pudendal)
external iliac supplies
anterior abdominal wall, lower extremities
schwannoma tumor marker
S-100 (both melanomas and schwannomas are S-100 because both are derived from neural crest cells)
schwannoma etiology
can come from any CN (except 2) because they’re all covered by schwann cells, tumors of PNS
schwannoma histology
biphasic pattern (antoni a + b), spindle cells (elongated with regular oval nuclei), highly cellular areas = antoni a, low cellularity = antoni b, antoni a areas may have palisading patterns = picket fence)
mitral stenosis from acute rheumatic fever
takes years or decades to develop, MCC mitral stenosis = chronic rheumatic fever
myocarditis from ARF
can cause dilated cardiomyopathy –> mitral regurgitation
acute rheumatic fever and PSGN
rarely occur together, caused by different strains