test #15 4.3 Flashcards
motor innervation of tongue?
hypoglossal CN XII, w/ exception of palatoglossus muscle CN X
general sensation of tongue?
anterior 2/3: mandibular branch of trigeminal (CN V3).
posterior 1/3: glossopharyngeal (CN IX).
posterior area of tongue root: vagus CN X.
gustatory innervation of tongue?
anterior 2/3: chorda tympani of facial n (CN VII).
posterior 1/3: glossopharyngeal CN IX.
posterior area of tongue root / taste buds of larynx and upper esophagus: vagus CN X
anterior 2/3rd of tongue vs. posterior 1/3rd?
terminal sulcus.
foramen cecum on tongue?
located along terminal sulcus at midline.
differentiate cystic fibrosis symptoms from kartagener?
both have (1) recurrent sinopulmonary infxn (2) infertility. but, kartagener has situs inversus
acetaminophen toxicity achieved when..
single dose of 250mg/kg bodyweight OR cumulative 24hr dose more than 12g/day
acetaminophen metabolism?
90% in liver by sulfation and glucoronide conjugation. remaining, oxidized via cytochromeP450 & urinary excretion of unmetabolized drug.
metabolite of acetaminophen metabolism by CP450 system?
NAPQI: toxic & highly reactive. usu metabolized by hepatic glutathione into non-toxic compounds.
acetaminophen toxicity
saturate hepatic sulfation&glucuronidation in liver; excess NAPQI made by CP450, depletion of glutathione. NAPQI causes hepatocellular injury and centrilobular necrosis
rx for acetaminophen toxicity. mechanism (2)
NAC (n-acetyl-cysteine). acts as glutathione substitute & (1) binds toxic NAPQI. also (2) provides sulhydryl groups to enhance non-toxic sulfation elimination of acetaminophen
aspirin (salicylate) & barbituate overdose rx?
(1) gastric decontamination (2) decrease GI absorption (3) correct fluid/electrolyte imbalance (4) alkalinize urine (increase excretion)
rx for TCA overdose?
NaHCO3; prevent cardiac arrythmia
opiod overdose rx?
opiod antagonist: naloxone or naltrexone
3 most common cancers in women?
(1) breast - low mortality (2) lung - highest mortality (3) colon. ovarian and cervical cancers have much lower incidence
which 2 vitamins are absent from breast milk? how do we manage this?
vitamin D and vitamin K. vitamin K given parenterally at birth (prevent hemorrhagic disease of new born). if baby dark, supplement vitamin D
cross-sectional study is also known as..
prevalence study. simultaneously measure exposure & outcome
filtration fraction determined by..
GFR and RPF (not saturable)
how is PAH secreted into urine?
clearance = RPF. filtered freely & actively secreted in PCT (carrier enzyme-mediated process aka saturable)
hallmark of reversible injury?
cellular swelling
how do mitochondrial react during irreversible injury?
vaculoization
CHF triggers what 3 compensatory responses?
(1) decreased GFR stimulates macula densa –> RENIN, angiotensin, aldosterone. (2) increased SYMPATHETIC output (baroreceptors perceive low perfusion). increased contractility (good) & HR (good), but also increase peripheral arterial resistance, which increases afterload (bad) (3) ADH, increased H20 retention, increased preload.
viscous cycle of CHF & renin & ADH
CHF –> bad pump, decrease perfusion to tissue. renin-angiotensin-aldosterone stimulated –> vasocontriction. increased afterload further impairs weak pump.
what type of CHF impairs cardiac output, systolic or diastolic
BOTH
the concentration of which 4 substances INCREASE as fluid runs along the PCT?
PAH, creatinine, inulin, urea (due to either active PCT secretion (PAH) or just nonreabsorption – concentrate bc water is reabsorbed)
the concentration of which 4 substances DECREASE as fluid runs through PCT?
greatest to modest decrease in conc: glucose, amino acid, bicarbonate (all reabsorbed in PCT)
the concentration of which 2 substances stay the same as fluid runs through PCT?
Na+ and K+ (bc travel w/ water)
incision layers for cricothyrotomy? between which two structures?
(1) skin (2) superficial cervical fascia (inclu subcutaneous fat and platysma) (3) investing and pretrachael layers of deep cervical fascia (4) cricothyroid membrane. between thyroid cartilage and cricoid cartilage.
buccopharyngeal fascia? acute necrotizing mediastinitis can be caused by..
extends from carotid sheath to invest the pharyngeal constrictor muscles. lies anterior to prevertebral fascia (forming retropharyngeal space between them). infxn involving the retropharyngeal space can extend directly into the superior mediastinum
vertebral location of cricoid cartilage?
C6 vertebrae
fascial layers of the neck (2 broad, with 4 subtypes)
(1) superficial cervical fascia. (2) deep cervical fascia: (a) INVESTING layer: surrounds neck like collar, inclu SCN, trap, & strap; submaxillary & parotid glands. (b) PRETRACHEAL: anterior park of neck, blends laterally w/ carotid sheath. encloses viscera of neck: thyroid, parathyroid, larynx, trachea, pharynx, esophagus (c) PREVERTEBRAL: surrounds vertebral column & muscles of spine. (d) CAROTID SHEATH: lies lateral to retropharyngeal space, deep to SCM, contains carotid artery, internal jugular vein & vagus n.
3 pathogenesis of hydrocephalus
(1) increased CSF production: rare; choroid plexus papilloma (2) abnormal CSF circulation; most common cause i.e. obstruction. (3) disorders of cerebrospinal fluid absorption: subarachnoid villi inflammation (i.e. subarachnoid/intraventricular hemorrhage or meningitis)
pseudotumor cerebri. classic demographic? sequelae?
idiopathic intracranial hypertension: elevated intracranial pressure w/ normal CSF content and normal neuro-imaging. usu young obese women. manifests as headache and papilledema: sequelae of optic nerve atrophy and blindness
transtentorial herniation results in..
herniation of parahippocampal uncus compresses ipsilat CN III and PCA. sign: fixed, filated pupil on same side as lesion
lissencephaly
agyria. congenital absence of gyri. accompanied by serve mental retardation.
theca externa vs. theca interna
theca externa: lies outside theca interna. does not participate in steroidogenesis. composed of a layer of smooth muscle and fibroblast cells. connective tissue support structure for follicle.
deltaF508 mutation in CF results in..
3-base pair deletion –> removes phenylalanine. results in IMPAIRED POST-TRANSLATIONAL PROCESSING (improper folding / glycosylation) of CFTR. detected by ER –> targeted for proteosomal degradation.
CF is characterized by which 3 things?
(1) recurrent sinopulmonary infxn (2) pancreatic insufficiency (3) gastrointestinal malabsorption
how is CFTR activated?
activated by cAMP-mediated phosphorylation and subsequently gated by ATP
transmission of hepatitis A
fecal-oral; common in areas w/ overcrowing / poor sanitation. contaminated water / food. RAW OR STEAMED SHELLFISH: common US culprit
clinical presentation of hepatitis A infxn
acute: malaise, fatigue, anorexia, nausea, vomiting, mild abdominal pain, AVERSION TO SMOKING. hepatosplenomegaly. elevated AST, ALT, bilirubin, ALP. self-limiting [3-6wks]. does NOT progress to chronic hepatitis, cirrhosis, HCC
close contacts of individuals w/ hep A?
immune globulin. high risk, should be given hep A vaccine as prophylaxis.
BNP
sign of CHF exacerbation: released in response to increased stretch. causes: vasodilation, diuresis/naturesis, decreased BP
S. pneumoniae vaccines (2)
(1) 23-valent polysaccharide single dose (older & asplenic) (2) 7-valent CONJUGATED vaccine (children less than 2)
two live vaccines used outside of US
(1) BCG: TB (2) typhoid vaccine: salmonella typhi
killed bacteria vaccines
anthrax, cholera, pertussis, plague
inactivated toxin vaccine (2)
(1) diptheria and (2) tetanus
galactose-1-P (and UDP glucose) —> UDP-galactose (and glucose 1 phosphate)
epimerization. galactose 1-phosphate uridyl transferase. deficiency in classic galactosemia.
UDP-galactose + UDP-glucose –> lactose (aka galactosyl beta-1, 4 glucose)
lactose synthase. occurs in breast tissue
classic galactosemia
impaired galactose-1-phosphate metabolsim
excess galactose in patients becomes.. (1)
(1) galactitol (galactose reductase) (2) galactonic acid (galactose oxidase). note: galactonic acid can be metabolized by HMP shunt. but, galactitol accumulates in cells –> irreversible eye & liver damage
action potential of pacemaker cells
phase 0: upstroke, L-type (long-lasting) DHP-sensitive calcium channels Ca++ channels.
phase 3: repolarization, opening of K+ channels and efflux of K+ ions form cell & closure of L-type Ca++.
phage 4: pacemaker potential; triggered by slow influx of Na+ after repolarization. also see decrease in K+ efflux as K+ channels continue to close.
when potential approaches -50mV, t-type (transient) Ca++ channels open, contributing to depol L type opens around -40mV. threshold around -40 and -30mV.
acetylcholine on pacemaker cells
parasympathetics: like adenosine, acts on phase 4 pacemaker potential. activates K+ channels (prolongs repolarization, increasing K+ conductance) AND decreases slow inward Ca++ during phase 4.
norepinephrine on pacemaker cells
facilitates opening of l-type Ca++ channels (and Na+) in phase 4 pacemaker potential, more rapid depolarization.
2 forms of vitamin K
(1) K1: phylloquinone, from green veggies and (2) menaquinone, from gut bacterial flora
why is vitamin K deficiency common in preterm newborns (4). not common in adults (2)
(1) hepatic immaturity (2) low vitK in breast milk (3) sterile GI tract (4) poor placental transfer of vit K.
not common in adults bc (1) widely available in plants (2) synthesized by gut flora
hemorrhagic disease of newborn
at risk if vit K def. characterized by cutaneous, GI, and intracranial bleeding. life threatening
CSF in bacterial meningitis
elevated opening pressure, increased neutrophils, decreased glucose, elevated protein
most common cause of bacterial meningitis in adults of ALL ages?
strep pneumoniae. lancet shaped gram positive cocci in pairs.
three most common causes of neonatal meningitis
(1) GBS (2) E. coli (3) Listeria
cluster headaches. demographics? onset?
rapid-onset, severe, nonpulsatile, unilateral periorbital & temporal pain, accompanied by nasal congestion, lacrimation, and ptosis. male 7x more likely. 30min-2hrs. around same time each day, consec days, for wks. usu at night, few hours after going to sleep. pain free interval of 1 yr between attacks
tension
bilateral, bank-like sensation of head, neck tightness. more common in women
migran w/o aura
severe, pulsatile, unilateral. exacerbated by physical activity. photophobia, phonophobia, nausea/vomiting
worst headache if my life
thunderclap – subarachnoid hemorrhage
subarachnoid hemorrhage
often, rupture of berry aneursym. can have meningeal signs
nonmalignant arterial HTN can present w/ what kind of headache
occipital morning headaches
characterize headaches associated w/ brain tumors
entire head, progress slowly over time, recumbent (on side) makes worse. accompanied by papilledema, vomiting, cognitive decline.
what is myeloperoxidase
blue-green heme-based pigmented molecule. found within azurphilic granules of neutrophils. produce hypochlorous acid (HOCl) from H2O2 and Cl. makes sputum green.
DHT is responsible for..
(1) develop external genitalia (penis and scrotum) in the embryo (2) growth of prostate (3) facial hair & temporal recession of hair line. DHT also amplifies testosterone effects.
2 types of 5-alpha-reductase. significance?
type 1: postpubescent skin. type 2: genitals. absence of type 2 associated w/ diminished DHT in tissues. absence of type 2 congenitally –> raised as female until puberty, when type 1 kicks in –> masculinization (male-pattern muscle mass, voice deepening, penile and scrotal growth, testicular descent)
lack of 5-alpha-reductase in male
pseudohermaphroditism, have male internal genitalia, but not external genitalia.
which 2 rxns does 21-hydroxylase mediate?
(a) 17-hydroxyprogesterone into 11-deoxycortisol (b) progesterone into 11-deoxycorticosterone
lead impairs what (2) enzymes in heme biosynthetic pathway
(1) delta-aminolevulinate dehydratase (ALA dehydratase) and (2) ferrochelatase
delta-aminolevulinate synthase (ALA-synthase). cofactor?
catalyze rate limiting rxn in heme synthesis. glycine + succinyl-CoA —-> d-ALA. cofactor –> B6
delta-aminolevulinate dehydratase (contains zinc)
2nd step in heme biosynthesis. 2 d-ALA –> pyrrole porophobilinogen.
ferrochelatase
final step in heme biosynthesis. Fe2+ incorportated into protoporphyrin IX
what accumulates (2) in lead poisioning?
(1) d-ALA and (2) protoporphyrin IX —> microcytic anemia
defects in uroporphyrinogen I synthase (HMB synthase). build up?
acute intermittent porphyria. acute attacks of abdominal pain and neurpsychiatric symptoms. no photosensitivty, but urine darks upon exposure to light. build up PBG (porphobillinogen).
defects in uroporphyrinogen decarboxylase causes? build up?
most common form of porphyria – porphyria cutanea tarda (PCT). uroporphyrinogen accumulates in urine. MILD PHOTOSENSITIVITY.
anti-TB intracellular agent? extracellular (i.e. organisms in necrotic foci and tissue cavities)
intracellular: pyrazinamide. extracellular – isoniazid, rifampin, ethambutol.
dopamine agonists (4). preferrentially stimulates..
ergot: (1) bromocriptine and (2) pergolide.
nonergot: (3) pramipexole (4) ropinirole
prefers D2 receptors.
rx for drug-induced parkinsonism; or tremor-predominant parkinsons?
anticholinergics (trihexyphenidyl and benztropine)
peripheral dopamine decarboxylase inhibitor?
carbidopa. blocks activation
COMT inhibitor
-capones
selegiline
MAO-B inhibitor (parkinsons)
systemic effect of COX-2 (2)
(1) fluid retention (renal vasculature. (2) block vascular endothelial cells & vascular smooth muscle production of prostacyclin PGI2, needed for anticoagualtion & vascular dilitation.
nodular and comedonal acne in 20s, esp in athelete?
20 – most outgrow acne associated w/ pubertal androgen surge. ANABOLIC STEROID USE (methyltestosterone)
methyltestosterone
anabolic steroid
pathophysiology of acne
(1) follicular epidermal hyperproliferation (2) excessive sebum production (3) inflammation (4) propionibacterium acnes
drugs known to cause acneiform eruptions (3)
(1) anabolic steroids, methyltestosterone (2) epidermal growth factor receptor inhibitors (3) lithium
ephendrine use
sympathomimetic agent related to methamphetamine. rx: bronchial asthma, stimulant, appetite suppressant, decongestant.
chewing tobacco associated w/ (4)
(1) dental caries (2) gingivitis (3) oral leukoplakia (4) oral cancer
UV light exposure predisposes to which dematoses (4)
(1) lupus (2) dematomyositis (3) pellagra (4) polymorphous light eruption. not associated w/ acneiform eruptions
perspiration on acne
exacerbates, but does not CAUSE ACNE
rx for chemo-induced vomiting? mechanism (2)
ondansetron, granisetron, dolasetron: (1) 5-HT3 receptor antagonist in chemoreceptor trigger zone. (2) block vagus-mediated nausea
describe vomit center (i.e. location of 5-HT3 receptors – 3)
GI tract, presynaptic vagal nerve terminals w/ 5-HT3 receptors that initiate vagus nerve activity in medulla oblongata’s “vomit center” (peripheral). central: 5HT-3 receptors in chemoreceptor trigger zone: AREA POSTREMA and SOLITARY NUCLEUS
n-acetylcestine
mucolytic, amphetamine toxicity (donate sulfhydryl group and binds NAPQI), and reno-protection (radiocontrast-induced nephropathy)
rx to minimize granulocytopenia after myelosuppressive chemo?
filgrastim (G-CSF)
prevention of anthracyclin-induced (i.e. doxorubicin) cardiotoxicity?
dexrazoxane: iron-chelator
decrease cumulative nephrotoxicity associated w/ platinum-containing and alkylating chemotherapeutics?
amifoxtine (cytoprotective free-radical scavenger)
prevention of tumor lysis (electrolyte disturbances and acute renal failure post chemo for a neuplasm w/ high cell turnover, like leukemia and lymphoma?
hydration, alkalinzation, allopurinol
cryptococcus neoformans path of entry
infects lungs – usu asymptomatic –> CNS
first step in patient with stroke
non contrast CT to see if ischemic or hemorrhagic. (clinially usu hemorrhagic: acute, focal deficits. ischemic: evolves fora few hours). hyperdensity –> hemorrhagic
most common cause of intraparenchymal hemorrhage
HTN. hyaline arteriolosclerosis in basal ganglia weakens walls, prone to dilation –> CHARCOT-BOUCHARD pseudoaneursyms. can rupture & bleed.
charcot-bouchard aneursyms vs. berry (saccular aneursyms)
Charcot-Bouchard: HTN, small arteries of basal ganglia and internal capsule, < 1mm, results in INTRAPARENCHYMAL hemorrhage in basal ganglia, internal capsule, thalamus, pons. sudden onset of FOCAL defecits.
berry (saccular) aneursyms: ADPKD, Marfan, Ehlers. circule of willis, anterior & posterior communicating, middle cerebral. variable size 2-25mm. rsults in SUBARACHNOID hemorrhage. sudden onset of headache & altered consciousness.
HTN encephalopathy refers to..
global symptoms caused by cerebral edema in patients w/ severe acute hypertension
most common cause of lobal parenchymal hemorrhage
cerebral amyloid angiopathy
alcoholic pancreatitis?
unclear pathophysiology: protein ppt within pancreatic ducts, calcify & obstruct.
intestinal bacterial overgrowth (bowel stasis, blind loops, extensive diverticulosis) results in steatorrhea bc…
bile salt deconjugation, failure of micelle formation
distinguish between acute renal failure & normal predictable rise in serum creatinine secondary to ACE inhibitor therapy
ACE inhibitors: increase in creatinine up to 30% within 2-5 days can be expected. stabilize in 2-3 wks. reversible on drug discontinuation
development of meningocele / anencephaly (embryologically)
neural folds –> neural tube, connected to amniotic cavity by openings at ends called anterior & posterior NEUROPORES. close during 4th wk of life. failure to close –> neural tube defect.
failure of neuropores to close cause what manifestations?
anterior closes 25th day. failure = anencephaly, encephalocele (protrustion of neural tissue through cranial defect).
posterior closes 27th day. failure = spina bifida occulta, meningocele, meningomyelocele, rachischisis (vertebrae arch never forms, spinal cord open)
how does chronic renovascular disease look on histology?
atrophic tubules
acute tubular necrosis: has lymphocytic infiltrate?
no, it’s acute. [though, acute rejection is characterized by lymphocytic infiltrate]
anti-CD3 antibodies
murromonab-CD3. anti-T cells. used for acute rejection in kidney, heart, and liver transplants
anti-epiderminal growth factor receptor? rx?
cetuximab. rx: non-small cell lung, colorectal, pancreatic, squamous cell carcinoma of head & neck.
anti-VEGF? rx?
bevacizumab. rx: metastatic colon, metastatic non-small smell lung, metastatic renal cell carcinoma and recurrent glioblastoma multiforme.
inspissated green fecal mass?
think: dehydrated meconium. results in meconium ileus.
bilious vomiting, abdominal distension, air fluid levels, and small bowel dilatation all indicate..
small bowel obstruction
most common cause of meconium ileus
cystic fibrosis. isotonic dehydration of luminal contents. secrete abnormally viscous mucous into the small bowel.
in US, 80% of deaths due to CF are related to..
cardiorespiratory complications. (pneumonia, bronchiectasis, bronchitis obstructive pulmonary disease, cor pulmonale)
diplopia when talking down stairs
think trochlear n. palsy (traumatic or idiopathic). vertical diplopia – when affected eye looks towards nose.
presentation of internuclear opthalmoplegia (MLF lesion)
impaired horizontal eye movement, weak adduction of affected eye w/ simultaneous abduction nystagmus of contralateral eye
crohn’s disease typically presentation?
abdominal pain & diarrhea in 20-30 year old. weight loss, fatiguabiity, low grade fever, apthous ulcers of oral mucosa.
transmural inflammation in crohn’s –> (2)
structures & fistulas
what’s involved in ulcerative colitis?
mucosa and submucosa only.
intramural gramulomas and skip lesions in Gi tract w/ cobblestone mucosa
crohn’s disease
toxic megacolon
neuromuscular degeneration of intestinal wall and rapid dilation. abdominal pain and distension. associated w/ bowel perfs, but not fistulas. life-threatening complication of crohn’s & ulcerative colitis.
intrasplenic lipid accumulation
seen w/ lysosomal lipid storage disorders like Gaucher’s disease
