test #22 4.12 Flashcards
signs of hypothyroidism
fatigue, weight gain, constipation, SLOWED RELAXATION of deep tendon reflexes, dry coarse skin
most sensitive marker for diagnosis of hypothyroidism
serum TSH
(though, will not be elevated in patients w/ hypothyroidism due to TSH deficiency [central hypothyroidism]
valproate teratogeniticty
neural tube defects (1-3% risk)
valproate inhibits intestinal folic acid absorption
signs of duodenal atresia?
clinical hallmark: bilious vomiting w/o abdominal distension. usually noted on 1st day of life.
peristaltic waves may be visualized in abdomen & history of polyhydramnios due to failure of amniotic fluid reabsorption in distal instestine
often seen in down syndrome
death resulting from bilateral renal agenesis
death from pulmonary hypoplasia shortly after birth
ebstein’s anomaly? cause?
atrialized right ventricle (downward displacement of tricuspid valve).
occurs when mom takes lithium early in pregnancy.
anaphylactic reaction to type O blood products in person w/ recurrent sinopulmonary and GI tract infections?
selective IgA deficiency.
anaphylaxis to IgA! make IgG against it. IgA = foreign
C1 esterase inhibitor deficiency
hereditary angioedema. rare. AUTOSOMAL DOMINANT. ace inhibitors are contraindicated.
C1 esterase inhibits nonspecific C1 fixation
delirium? causes?
delirium: ‘waxing & waning’ fluctuations in consciousness. acute, global memory impairment, visual hallucinations. ‘altered sensorIUM’
reversible & commonly occurs in hospital setting
AEIOU TIPS:
alcohol, electrolyte imbalace, iatrogenic (i.e. meds), oxygen hypoxia, uremia. trauma, infxn, posion, seizure (post-ictal)
delirium vs. dementia
onset, consciousness, course, prognosis, memory
in delirium:
acute, impaired consciousness, fluctuating symptoms, reversible, GLOBAL memory loss.
in dementia:
gradual, intact consciousness, progressive decline, usu irreversible, remote memory SPARED.
(reversible, at least partially, with: NPH, vitamin b12 deficiency, hypothyroidism, neurosyphilis, HIV)
Reye’s syndrome description and pathogenesis
hepatic failure and acute encephalopathy. associated w/ use of aspirin in patients 5-14 y/o.
pathogenesis: unknown; affected children have metabolic error sensitizing to toxic effect of salicylates. especially in virally-infected cells. causes mitochondrial dysfunction.
mechanism: aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes.
describe lab findings & histology in reye’s
vomiting, hepatomegaly. jaundice = rare.
increased ALT, AST, ammonia, bilirubin, prolonged PT and PTT.
light microscope: microvesicular steatosis. NO necrosis or inflammation.
EM: swelling, decreased mitochondria, glycogen depletion.
do not give aspirin (salicylates) to kids under..
16 y/o (except if Kawasaki)
histology of viral hepatitis
apoptosis of hepatocytes, acinar necrosis, periportal mononuclear inflammatory infiltration
liver findings in patients w/ right-sided heart failure
centrilobular congestion
histology of primary biliary cirrhosis
bile duct destruction, periductal granulomatous inflammation, bile duct proliferation
respiratory epithelium with stratified squamous epithlium
response to chronic irritation: METAPLASIA.
adaptive: resistant to irritation than columnar cells.
HOWEVER: no cilia/goblet cells: no mucociliary clearance. can lead to dysplasia (low-grade atypical cells). risk factor for carcinoma (high-grade atypia).
REVERSIBLE, can resolve upon discontinuation of smoking.
renal response to markedly narrowed renal artery (i.e. stenosis)
compensatory RENIN secretion (juxtaglomerular apparatus)
eventually: juxtaglomerular apparatus undergoes hypertrophy & hyperplasia (to make more renin).
juxtaglomerular apparatus: JG cells and macula densa
juxtaglomerular cells: modified SMOOTH MUSCLE CELLS located in alls of afferent and efferent arterioles.
macula densa: tall, narrow cells in distal tubules. monitor osmolarity and volume of urine that passes into distal tubules. pass info to JG.
juxtaglomerular apparatus (2)
juxtaglomerular cells: modified smooth muscle cells in afferent & efferent arteriole. secrete RENIN.
macula densa: tall narrow cells in distal tubules, sense osmolarity & volume in tubules
noise-induced hearing loss?
trauma to sterociliated hair cells of organ of orti. >85dB. distortion / fracture of stereocilia due to shearing forces against tectorial membrane.
loose high frequency first (4000Hz)
frequency of speech
500-3000Hz
acoustic reflex?
dampens effects of prolonged loud noise by contracting stapedius & tensor tympani.
tensor tympani & stapedius
note. paralysis of mandibular CNV3 results in hypoacussis – complete loss of tensor tympani tone = hard to hear (even though it normal fxn dampens sounds at other extreme).
loss of stapedius (CNVII) = hyPERacussis
cupula
lies at apex of cochlea. has cells that sense rotation.
enhance LVOT in HCM by.. (3)
decreases venous return (valsalva, standing suddenly).
decreasing afterload.
increasing contractility
referral bias
/ admission rate bias. when cases & controls differ due to admission / referral processes.
i.e. enroll patients from all over nation, but use hospitalized control subjects form local institution
detection bias
a risk factor itself may lead to extensive diagnostic investigation & increase probability that disease is identified.
i.e. detecting more cancer in smokers, but smokers have more imaging surveillance due to smoking status!
sampling bias
non-random sampling of population. lead to study population having characteristics different from target population.
severely ill patients are more likely to enroll in cancer trials – so results may not be applicable to patients w/ less advanced cancer.
lightning-related complications (5 systems)
(1) cardiac: arrest, arrhythmia
(2) neurologic: perihperal n. damage, seizure, confusion, respiratory arrest, autonomic dysfxn.
(3) dermatologic: lichtenberg figures (pathognomonic of lighting strike)
(4) MSK: rhabdomyolysis, bone fracture, compartment syndrome
(5) cataractsery (late sequelae), ruptured tympanic membrane, curling ulcers.
erythematous cutaneous marks in a fern-leaf pattern & second degree burns..
lichtenberg figures – LIGHTNING INJURY
why are deep tissue burns relatively rare post-lightning strike?
short duration of electrical contact & flashover effect: tendency of lightning to travel over skin surface and discharge on ground –> lichtenberg figures
how does lightining cause skeletal fracturs?
rapid heating of surrounding air, generating shock waves, can travel through body & cause mechanical trauma.
rules re: cardiac pressure
- left > right
- atria ~ 10mmHg max.
- max pressure in right ventricle & pulmonary artery ~ 25mmHg.
- max pressure in aorta & LV ~ systolic BP
normal pulmonary pressure at rest? pulmonary HTN at?
at rest: 10-14mmHg.
pumonary HTN > or equal to 25mmHg.
protein A. protein cell wall component (a single polypeptide chain)
- staph aureus
- binds to Fc region of IgG, causing epitope binding sites to face AWAY from bacteria. prevents complement fixation and phagocytosis
sounds from opening snap in mitral stenosis
abrupt halting of leaflet motion during mitral valve opening (due to fusion of mitral valve leaflets).
most common cause of mitral stenosis
prior rheumatic carditis
secretin S cells located…
duodenum. increase bicarb secretion from exocrine pancreas. stimulated by HCl in duodenum.
role of thyroglobulin peroxidase (3)
(1) oxidation of inorganic iodine
(2) formation of mono- and diiodotyrosine
(3) coupling that forms T3 and T4.
thyroglobulin
high molecular weight, glycosylated protein that is present within the thyroid follicle. TSH increases its gene transcription.
role of thyroglobulin
iodine is added to tyrosine residues on thyroglobulin & stored there until thyoid follicular cells engulf, cleave for use.
how does N. meningitidis get into the meningies
pharynx –> bloodstream –> choroid plexus —> meninges
remember hematogenous bc of systemic signs (i.e. sepsis & characterestic petechial signs, waterhouse-friderichsen, etc)
how does haemophilus influenza get into the meninges?
pharynx –> lymphatics –> meninges
how can S. pneumonia get to meninges post0otitis media?
middle ear –> contiguous tissues –> meninges
how does s. pneumonia and TB from lungs get into meninges?
primary lung focus –> blood –> meninges
describe TB meningitis
chronic, characterized by monoctes & lymphocytes in CSF, primarily affecting BASAL meninges.
typical adenovirus presentation
pharyngoconjunctival fever.
acute, self-limited, febrile pharyngitis cough, nasal congestion, conjunctivitis, enlarged cervical nodes.
accounts for only 2-4% of acute viral illnesses in general population, but common in crowded quarters (barracks, camp)
calicivirus
Norwalk virus – epidemic outbreaks of viral gastroenteritis
bronchiolitis in infants caused by
RSV (paramyxovirus)
arenavirus
lymphocytic choriomeningitis virus (LCV). febrile aseptic meningoencephalitis or milk systemic influenza-like illness in humans exposed to infected HAMSTERS or MICE. (not person-to-person)
transport of unconjugated bilirubin into hepatocytes?
transported of conjugated bilirubin out of hepatocytes?
indirect unconjugated bilirubin. PASSIVE. via organic anion transporting polypeptide (OATP).
secreted ACTIVE via an ATP-binding cassette protein MRP2.
(if impair MRP2, conjugated bilirubin can passively diffuse via basolateral OATP –> conjugated hyperbillirubinemia.
describe conjugated bilirubin.
unconjugated bilirubin.
water soluble, non-toxic, loosely bound to albumin. can be excreted in urine.
unconjugated bilirubin: insoluble in water at physiological pH, tightly complexed to albumin. cannot be excreted in urine.
which type of bilirubin can lead to jaundice?
BOTH unconjugated & conjugated (bilirubin glucuronides) can accumulate systemically and deposit in tissues –> jaundice.
