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histology of true vocal folds

stratified squamous epithelium


- regions of respiratory tract with ciliated, pseudostratified, columnar, mucus-secreting epithelium
- regions with stratified squamous epithelium

- paranasal sinus, nasopharynx, most of larynx (including false cords), tracheobronchial tree
- oropharynx, laryngopharynx, anterior epiglottis, upper half of posterior epiglottis, true vocal cords


HIV fusion depends on...

(1) host cell CD4 + CCR5 and (2) HIV gp120


Nef and Tat HIV gene

Tat: role in viral replication
Nef: decreases expression of MHC class I on surface of expressed cells


When does tetrology of fallot present w/ cyanosis?

when pulmonic stenosis results in enough pulmonary HTN to turn VSD into a right-to-left shunt


Endocardiac cushion defects result in

defects in atrioventricular septum (left-to-right shunt, initially asymptomatic, but can have Eisenmenger syndrome later on


3 major cyanotic diseases caused by abnormal migration of neural crest cells...

tetralogy of fallot (anterior misalignment of aorticopulmonary septum), transposition of great vessels, truncus arteriosus


(3) mitochondrial myopathy (blotchy red muscle fibers on Gomori trichrome stain)

(1) myoclonic epilepsy w/ ragged red fibers [MERRF] (2) leber optic neuropathy [blindness] (3) mitochondrial encephalopathy w/ stroke-like episodes and lactic acidosis (MELAS)

ragged red bc abnormal mitochondria deposit under sarcolemma


Inheritance of cystic fibrosis

autosomal recessive (chr. 7)


fertility w/ cystic fibrosis

most men are infertile, but not sterile


human multidrug resistance (MDR1) gene

codes for P-glycoprotein, a transmembrane ATP-dependent efflux (esp good for hydrophobic agents like anthracyclines)

prevents influx as well as increases efflux


What precipitates sickling in HbS?

low oxygen, increased acidity, low volume (dehydration) [valine instead of glutamate at 6th AA position in beta subunit


hemoglobin M disease

mutation in heme binding pocket of alpha or beta chain; most common mutation replaces histidine in the heme binding pocket with tyrosine, results in the formation of an iron phenolate complex that resists the reduction of iron to the ferrous state --> methemoglobin


Wilson's disease

decreased ceruloplasmin


lipid loss in nephrotic syndrome under microscopy

polarized light -> oval fat bodies have maltese cross appearance


high altitude acclimatization process

inspired partial pressure (pO2) falls from 150 to 86mmHg, resulting from PaO2 of 60mmHg or less. hypoxemia stimulates carotid & aortic body chemoreceptors --> increased ventilatory drive --> hyperventilation and respiration alkalosis (increased pH, decreased CO2, low O2). drop in bicarb within 48 hours. within hours, increased EPO. see increased RBC 10-14 days. also, increased capillary density, myoglobin concentration, mitochondria


describe osteoclasts in paget's disease of the bone

very large, can have up to 100 nuclei (normal 2-5). will be tartrate-resistant acid phosphatase positive (like all osteoclasts)


factors important for osteoclastic differentiation

(1) M-CSF (macrophage colony-stimulating factor) and (2) RANK-L (receptor for activated nuclear factor kappa beta-ligand)


typical presentation of Paget's disease of bone

older gentleman, pain and deformity in a bony area and hearing loss (conductive problem w/ bone) . potentially caused by paramyxovirus infxn of osteoclasts


fibroblast growth factor on bone

increase bone formation, stimulate osteoblast. neurovascularization and wound healing


TGF-beta on bone formation

increases replication of osteoblast precursors and increased formation of mature osteoblasts. increase collagen synthesis. stimulate osteoclast apoptosis; decrease bone resorption


insulin-like growth factor on bone formation

IGF-1 increases osteoblast replication and collagen synth. decreases collagen degradation; inhibits MMP-13. anabolic


osteocalcin in bone formation

non-collagenous protein secreted by osteoblast. marker of bone formation. limits bone mineralization.


factors that stimulate osteoblasts



pulsus paradoxus (definition, detection, pathophysiology)

decrease in systolic BP greater than 10mmHg on inspiration. korotkoff sound first heard on expiration, then later on all phases of respiration.

caused by IMPAIRED expansion in PERICARDIAL space

normally, inspiration increases venous return --> increased volume of right heart, which expands into pericardial space.

when impaired expansion (acute cardiac tamponade, constrictive pericarditis, severe obstructive lung disease, restrictive cardiomyopathy)

here: increased RV volume pushes interventricular septum to left, reducing left heart diastolic volume & stroke volume --> decreases systolic BP.


Parvovirus B19

the only ss DNA virus (non-enveloped)


beta-hemolytic bacteria

s. aureus, listeria monocytogenes, s. pyogenes, s. agalactiae


listeria monocyogenes characterestics

- tumbling motility at 22 deg (immobile at 37)
- can multiply at 4 deg (refrigeration)
- only gram positive with LPS!


intracellular evasion strategies of Salmonella & Mycobacterium

- block fusion of phagolysosome with lysosome
- tuberculosis also blocks phagolysosome acidification


rheumatic fever on heart valves

almost always affects mitral, but both mitral and aortic are affected in some. often combined aortic stenosis and regurgitation, both --> increased LV diastolic pressure. predispose to infective endocarditis.


branched-chain alpha-ketoacid dehydrogenase, pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase all require which five cofactors?

thiamine pyrophosphate, lipoate, coenzyme A, FAD, NAD (mnemonic: tender loving care for nancy)


describe path of pulmonary artery post bifucation (relative to aortic arch, SVC, left main bronchus)

pulmonary trunk is to the left of aortic arch. right pulmonary artery travels under aortic arch and posterior to SVC. left pulmonary artery travels superior over left main bronchus


at what costal cartilage level does SVC form

1st costal cartilage


presentation of complete hydatidiform mole

bunch of grapes, result of trophoblast proliferation. large villi with decrease villous blood vessels.

vaginal bleeding in first trimester
nausea and vomiting
excessive hcg -> theca-lutein cyst


prognosis of complete hydatidiform mole

most recover after removal. some progress to 1. invasive mole (penetrate uterine wall; hydropic villi and proliferated trophoblast) or 2. choriocarcinoma (malignancy of trophoblastic cells; atypical cyto and synctiotrophoblastc w/ focal hemorrhage and necrosis).


elevated AFP in pregnant woman suggests.. (4 things, 1 main)

fetal neural tube defect
underestimation of gestational age
abdominal wall defect


CEA is a marker for

colorectal carcinoma


formula for confidence interval

mean +/- 1.96*SD/sqrt n

SEM = SD/sqrt n
95% confident that the true mean of the underlying population falls in this interval (1 z-score)

mean, SD, z-score, sample size


examples of signals using receptor-tyrosine kinase

growth factor receptors: EGF, PDGF, FGF


examples of tyrosine-kinase ASSOCIATED receptors (JAK/STAT)

cytokines, growth hormone, prolactin, IL-2, colony-stimulating factors


ANP signaling receptor

intrinsic guanylate cyclase activity


what can arginine deficiency be confused with (clinical presentation)?

cerebral palsy, progressive spastic paresis. arginine deficiency -- build up of arginine, can't make urea and ornithine. rx: low arginine diet


synthesis of 5-HT

hydroxylation and decarboxylation of tryptophan by tryptophan hydroxylase


role of glutamate in the body

transports ammonia from peripheral tissues to kidney. in nephron, hydrolyzed by glutaminase to generate glutamate and free ammonium


orotic acid build up when

block in urea acid cycle; ornithine transcarbamylase deficiency (OTC), citrullinemia, and argininosuccinic aciduria


vitamin B6, B12, and folate deficiency are associated with high levels of what compound?

homocysteine --> associated with atherosclerosis and thrombotic events


formation of GABA

decarboxylation of glutamate by (GAD) glutamic acid decarboxylase



mature defense, where unacceptable drive/emotions redirected towards acceptable targets (rage -> gym)
vs. displacement, where redirected towards unacceptable targets (rage -> wall, pets)


reaction formation

immature defense, unacceptable feelings are ignored and opposite sentiment is adopted. (i.e. man is angry at wife, but instead compliments dress)


most impt virulence factor in e.coli UTI

Fimbriae, or pili (specifically P-fimbriae = pyelonephritis-associated pilli). permits adhesion


most impt virulence factor in e. coli meningitis

K1 capsulate antigen


lipid A

component of lipopolysaccharide in enterobacter --> activation of macrophages, widespread release of IL-1, IL-6, TNF-alpha


outflow murmur with HCM

systolic anterior motion of mitral valve touches hypertrophied inter ventricular septum


inspiration effect on right and left heart

RIGHT: INCREASED venous return to right atrium --> increased volume in right ventricle. increase

LEFT: pulmonary vessel capacitance, DECREASING venous return to left ventricle


differentiate tricuspid regurg vs. mitral regurg vs. VSD

1. inspiration increases tricuspid intensity (MR and VSD don't)
2. location:
- tricuspid loudest near left lower sternal border
- mitral loudest over cardiac apex (high pitched)
- VSD loudest over left sternal border bet 3/4th intercostal space


systolic murmurs

- aortic stenosis: midsystolic, crescendo-decrescendo, travels to clavicle
- mitral regurg: holosystolic, high-pitched, LLD, apex
- tricuspid regurg: inspiration increases intensity, left lower sternal border
- pulmonic stenosis
- VSD: holosystolic blowing murmur, left sternal border 3/4th intercostal space


diastolic murmurs

- aortic regurg:
- mitral stenosis: mid-diastolic, low pitched murmur, starts after S2 and ends before S1
- tricuspid stenosis:
- pulmonic regurg: inspiration increases intensity early diastolic, starts w/ S2, ends before S1 (decrescendo), high-pitched blowing best heard over left 2nd and 3rd space
- ASD:


Tricyclic antidepressants receptor targets (5)

1. central and peripheral mAch-R
- tachycardia, delirium, dilated pupils, flushing, decreased diaphoresis, hyperthermia, intestinal ileus, urinary retention
2. peripheral alpha-1-adrenergic receptors
- peripheral vasodilation (orthostatic HTN)
3. cardiac fast Na+ channels
- conduction defects, arrythmia, hypotension
4. presynaptic NE 5HT ntx reuptake
seizure and tremors
5. histamine H1 receptor


most common cause of death in patients w/ antidepressant intoxication



what mediates cachexia?

TNF (along w/ sepsis)


death due to TCA toxicity results from.. Rx is..

primarily blockade of fast Na+ channels --> ventricular fibrillation and/or cardiogenic shock. Rx: fluid resuscitation w/ normal saline and hypertonic sodium bicarb


presentation of serotonin syndrome

hyperthermia, autonomic instability, muscle rigidity, myoclonus, diaphoresis


impairment of respiratory control centers in brainstem (ondine's curse)

decreased frequency and/or amplitude of involuntary respiratory result in respiratory arrest when sleeping. (voluntary breathing unaffected)


progressively weakening diaphragmatic contractions during ventilation w/ intact phrenic can be (2)

NMJ problem (myasthenia gravis) and/or abnormally rapid diaphragmatic muscle fatigue (restrictive lung / chest wall disease)


angiotensin II receptor blockers act on..

AT-1 (angiotensin II receptors); block constriction of vascular smooth muscle & block aldosterone secretion. also block negative feedback of renin, angiotensin I, angiotension II


alpha-1-adrenergic mediated vasoconstriction affects... (2)

skin and viscera (i.e. reduces renal and hepatic blood flow)


NE affects (2)

1. a1 -> vasoconstriction, increase systolic/diastolic BP
2. b1 -> increase cAMP. would imagine increase in contractility, conduction, and chronotropic effects, but counteracted by indirect baroreceptor-mediated reflex bradycardia (no change or even decrease)


what are some potential benefits of ACE inhibitors? when are ACE inhibitors contraindicated?

reduce mortality risk in patients w/ cardiovascular and peripheral vascular disease, decrease LV vol in aortic regurg, reduce infarct expansion & progressive LV remodeling post-infarct.

contraindicated in pts w/ extensive atherosclerotic disease & bilateral renal artery stenosis; ATII-mediated vasoconstriction of efferent arteriole is essential for GFR maintenance here


conus medullaris syndrome (vertebral level & clinical presentation)

L2 vertebral level; damage to cord; flaccid paralysis of bladder and rectum, impotence, and saddle (S3-S5) anesthesia (disk herniation, tumor, spinal fractures) can also have mild leg muscle weakness


cauda equina syndrome

results from massive rupture of an intervertebral disk capable of compressing 2+ (of the 18) spinal nerve roots. can be from any trauma/space occupying lesion.

involved in: sensory & motor of lower extremities, pelvic floor, sphincters

classic symptoms: low back pain radiating to one or both legs, saddle anesthesia, loss of anocutaneous reflex, bowel/bladder dysfunction (S3-S5), loss of ankle-jerk reflex with plantar flexion weakness of feet.


pudendal nerve

S2-S4, perineum


femoral nerve

L3 L4, mediate quadriceps (knee-jerk/patellar reflex)


achilles reflex

s1 and s2


when should you test serum cortisol for cushing?

evening, since cortisol should be low in most people (circadian rhythm) more sensitive and specific


gold standard diagnosis for mesothelioma & features that distinguish it from adenocarcinoma.

clinical presentation of mesothelioma?

EM; numerous slender microvilli w/ abundant tonofilaments

(as opposed to adenocarcinoma -- short, plump microvilli)

dyspnea and chest pain. hemorrhagic pleural effusion and pleural thickening


bronchoalveolar carcinoma on chest x-ray

variant of adenoarcinoma in periphery of lung. peripheral mass or area of pneumonia-like consolidation


distinguish small cell and squamous carcinoma (2 similarities, 1 distinguish) on X-ray and staining

1. both arise form major bronchi 2. both will appear as hilar mass 3. small cell stains for neuroendocrine markers like chromogranin and synpatophysin, squamous stains for keratin and intercellular bridges.


how do thiazides cause hypokalemia (2 mechanisms?) hyperglycemia? hyperuricemia? hypercalcemia?

hypokalemia: 1. increased delivery of Na+ to CT 2. volume contraction stimulates aldosterone secretion, which increases K+ excretion
--> leads to muscle weakness & ECG problems

hyperglycemia: decreased insulin secretion & glucose uptake by tissues

hyperuricemia: hypovolemia increases uric acid reabsorption in PCT

hypercalcemia: increase calcium reabsorption


Rx: idiopathic hypercalciuria / recurrent calcium stone nephrolithiasis

thiazide diuretics; increase Ca++ reabsorption in DCT


clinical presentation with hyperphosphatemia?

like hypokalemia: muscle weakness and paralysis. commonly seen in alcoholics


renal blood flow formula

RBF = (PAH clearance / 1- hct)


chi-square test vs. two-sample z or t-test vs. ANOVA

test for independence; test for association between 2 categorical varibles; whether the expected freq of an occurrence is consistent with the observed frequency of occurrence, "goodness of fit", i.e. mendelian inheritence

two-sample t or z test compares MEANS of 2+ groups

ANOVA: means of 2+ groups