test #10 3.24 Flashcards Preview

UWorld mixed > test #10 3.24 > Flashcards

Flashcards in test #10 3.24 Deck (136)
Loading flashcards...
1
Q

major component of pulmonary surfactant? released triggered by?

A

dipalmitoyl phosphatidylcholine; calcium dependent fusion of lamellar body membrane w/ type II pneumocyte cell membrane.

2
Q

what can cause bronchoconstriction (5)?

A

(1) alveolar hypocapnia, (2) bronchial inflammation, (3) parasympathetic (cholinergic) (4) efferent nerve activity, and (5) inhaled / aspirated irritants

3
Q

bladder carcinomas are often (1)? which (2) are possible, but rare?

A

urothelial (transitional cell) carcinomas compose 90% of malignant bladder neoplasms. squamous cell and adenocarcinomas are rare.

4
Q

classic presentation of bladder carinoma

A

painless gross hematuria. mass grows as papillary or sessile mass.

5
Q

diagnosis of bladder carcinoma

A

cystoscopy

6
Q

squamous cell carcinoma of bladder is associated with..

A

rare; associated w/ schistosoma haematobium infection

7
Q

best predictor of malignant potential of bladder carcinoma?

A

tumor stage / penetration of bladder wall

8
Q

biotin serves as..

A

CO2 carrier on surface of carboxylase enzyme. (encompasses enzymatic subtypes acetyl-CoA carboxylase [ACC], pyruvate carboxylase [PC], propionyl carboxylase [PCC], beta-methylcrotonyl CoA carboxylase). important in carbohydrate and lipid metabolism.

9
Q

biotin deficiency can cause what two metabolic derangements

A

(1) metabolic acidosis: in tissues responsible for gluconeogenesis, pyruvate carboxylase (and biotin) is needed for conversion of pyruvate to oxaloacetate. in deficiency, pyruvate levels rise and converted to lactic acid instead. (2) fatty acid excess: propionyl CoA carboxylase (and biotin) needed to synthesize succinyl CoA from amino acids like valine. biotin-deficient –> propionyl CoA builds up and instead metabolized into surplus of odd-chain fatty acids.

10
Q

biotin deficiency results from.. (3)

A

poor diet, excessive raw egg white consumption (high levels of biotin-binding avidin in egg whites) and congenital disorders of biotin metabolism

11
Q

delayed puberty + anosmia

A

Kallmann syndrome. failure of GnRH neurons to migrate from origin in olfactory placode (situated outside CNS) to normal anatomic position in hypothalamus. will have some pubic hair bc normal adrenarche occurs normally

12
Q

mutation in Kallmann syndrome (2)

A

KAL-1 gene or the FGFR-1 gene (required for GnRH neuron migration)

13
Q

US definition of delayed puberty in boys & girls

A

absence of incomplete development of secondary sexual characteristics by 14 in boys and 12 in girls.

14
Q

first sign of puberty in boys? girls?

A

testicular enlargement in boys. breast enlargement in girls.

15
Q

megaloblastic anemia w/ peripheral neuropathy

A

cobalamin deficiency. (folate alone cannot cause peripheral neuropathy)

16
Q

usage of folate alone w/ B12 deficiency?

A

can moderately improve hemoglobin levels, but will worsen demyelination & abnormal myelin synth by depleting concentration of unmethylated cobalamin available for methymalonyl-CoA processing.

17
Q

high dose folate can have what drug interaction

A

may antagonize phenytoin

18
Q

major cause of abdominal aortic aneursym?

A

atherosclerosis. intimal fatty streaks –> progress enough to weaken underlying media of aortic wall.

19
Q

intimal fatty streaks

A

earliest lesion of atherosclerosis – intimal lipid-filled foam cells, derived from macrophages and SMCs that have engulfed LDL.

20
Q

medial degeneration

A

characterized by fragmentation of elastic tissue and separation of the elastic and fibromuscular components of tunica media by small, cleft-like spaces. less common than atheroscerlosis

21
Q

medial inflammation

A

results in arteritis (i.e. giant cell or takayasu). can promote aortic aneursym, but rare

22
Q

dense periaortic fibrosis w/ inflammatory reaction

A

unusual variant of abdominal aortic aneursym, rich in lymphocytes, plasma cells, macrophages, and often giant cells. unclear cause.

23
Q

squamous cell carcinoma of the anus

A

pain, itch, rectal bleeding, visible ulcerative mass. linked to HPV infection w/ 16 and 18.

24
Q

reactivation of EBV in HIV+ can manifest as.. (2)

A

(1) non-hodgkin’s lymphoma and (2) oral hairy leukoplakia [white plaques on lateral tongue margins]

25
Q

presentation of lymphogranuloma venereum

A

ulcerative / vesicular lesion on external genitalia –> regional PAINFUL lymphadenopathy. could have proctitis w/ tenesmus and bloody discharge. not common.

26
Q

aortic dissection A vs. B

A

type A: any portion of the ascending aorta. type B: descending aorta.

27
Q

aortic dissection blood pressure discrepancy?

A

as dissecting intramural hematoma spreads along aortic wall can compress major arterial branches

28
Q

primary risk factor for aortic dissection. describe pathogenesis

A

hypertension (medial hypertrophy of aortic vasa vasorum, consequently, reduced blood flow to aortic media. can cause medial degeneration w/ loss of smooth muscle cells –> aortic enlargement and increased wall stiffness. exacerbate aortic wall stress. synergistic increase in aortic WALL STRESS greatly increases risk of INTIMAL tearing & blood entering dissect through MEDIA.

29
Q

monckeberg sclerosis (medial calcific sclerosis)

A

form of arteriosclerosis characterized by calcific depositis in MEDIAL layer of MUSCULAR arteries. usu pts > 50y/o. can cause isolated systolic HTN due to arterial hardening.

30
Q

severe megaloblastic anemia precursors

A

90% of erythroid precursors are destroyed w/o ever entering circulation. bone marrow is hypercellular

31
Q

can peripheral neuropathy in B12 deficiency occur in the absence of frank anemia?

A

YES! and folate can make neuro symptoms worse.

32
Q

MCV > 100 fL? MCV > 110?

A

MCV > 100 can be seen with liver disease, hypothyroidism, alcoholic liver disease, and B12/folate def. MCV > 110 typically only seem w/ B12 and folic acid deficiency.

33
Q

consumption of fish in japanese restaurant? symptoms? rx?

A

think pufferfish – TTX ingestion (block voltage-gated sodium channels) symptoms: dizziness, weakness, loss of reflexes, paresthesia of face and extremities, nausea, vomiting, diarrhea, severe hypotension, general paralysis, death. rx: supportive care & intestinal decontamination w/ gut lavage and charcoal.

34
Q

what are 4 toxins that block voltage gated Na+ channels? by what mechanism?

A

(1) tetrodotoxin (puffer-fish) (2) saxitoxin (dinoflagellates in “red tide”) —-> 1 & 2 bind Na+ channels and inhibit Na+ influx, preventing AP conduction.
(3) ciguatoxin (exotic fish, Moral eel) (4) batrachotoxin (south american frogs) —–> 3 & 4 bind to Na+ channels and deep open, causing persistent depolarization.

35
Q

power. positively correlated with what?

A

the probability of seeing a difference when one truly exists (1-beta) beta = probability of being blind to a true difference. power is positively correlated w/ SAMPLE SIZE

36
Q

foamy, frothy urine caused by.. (2)

A

proteinuria or bile salts in urine

37
Q

most common cause of coronary sinus dilatation?

A

elevated right-sided heart pressure secondary to pulmonary artery HTN. usu coronary sinus is not visible.

38
Q

5 causes of accelerated bone loss (which can lead to pathological fractures)

A

(1) hyperprolactinemia –> hypogonadism (2) hyperparathyroidism (3) hyperthyroidism (4) chronic glucocorticoid excess (5) vitamin D deficiency

39
Q

stomach ulcers can occur w/ which 2 things?

A

(1) isolated hyperparathyroidism or (2) Zollinger-Ellison syndrome

40
Q

purposeless extremity movement w/ restlessness 3 months after a sore throat?

A

Sydenham chorea (most common acquired chorea of childgood, sole neurologic manifestation of acute rheumatic fever) hyperkinetic extrapyramidal movement disorder.

41
Q

sydenham chorea caused by… abs?

A

CNS autoimmune reaction precipitated by group A beta-hemolytic strep throat after 2-3 month latency. anti-neuronal antibodies binding to caudate and subthalamic nuclei.

42
Q

chronic rheumatic heart disease

A

mitral and aortic valve involvement

43
Q

major and minor jones criteria for diagnosis of acute rheumatic fever

A

2 major. or 1 major & 2 minor. major: polyarthritis (joint), carditis, subcutaneous nodules, erythema marginatum, sydenham chorea. minor: fever, arthralgia, elevated acute-phase reactants (ESR or CRP), prolonged PR

44
Q

polyarthritis in acute rheumatic fever

A

migratory & transient. rarely, if ever, deforming!

45
Q

3 ways kidney corrects disturbances in acid-base balance

A
  1. excess H+ excreted 2. bicarbonate recycled [carbonic anhydrase in proximal tubule lumen combines H+ & HCO3- —> H2CO3 —> H20 and CO2 (reabsorbed by epithelial cells) –> in cell, H2O and CO2 rejoin to make H2CO3, which dissociates into H+ and HCO3-. HCO3- is reabsorbed, H+ is returned to lumen. 3. titratable acids are excreted {limit to urinary excretion of free H+ (pH 4.5), some H+ is bound by HPO4- and NH3 to form titratable acids H2PO4- and NH4+. allows for excretion of acid w/o rapid decrease in urinary pH
46
Q

minimum urinary pH

A

limit to urinary excretion of free H+. pH = 4.5

47
Q

stab in left sternal border, fourth intercostal space (level of nipple)

A

(1) skin and subcutis (2) pectoralis major muscle (3) external intercostal membrane (4) internal intercostal muscle (5) internal thoracic artery and veins (6) transversus thoracis muscle (7) parietal pleura (8) pericardium (9) right ventricular myocardium

48
Q

how could one stab the IVC?

A

stab wound to the back immediately to the right of the vertebral bodies

49
Q

most common inborn error of methionine metabolism?

A

homocystinuria

50
Q

presentation of homocystinuria

A

present at 3-10y w/ ectopia lentis (dislocated lens). about 1/2 experience intellectual disability. marfanoid habitus (elongated limbs, arachnodactyly, scoliosis) and osteoporosis. high risk for thromboembolic episodes involving both large and small vessels (esp brain, heart, and kidney).

51
Q

major cause of morbidity and mortality in homocystinuria?

A

thromboembolism

52
Q

most freq cause of homocystinuria?

A

deficiency in cystathione synthetase (requires pyridoxine B6 as a cofactor).

53
Q

rx for homocystinuria

A

many respond dramatically to pyridoxine B6 supplementation (improves residual enzymatic activity and reduces plasma homocysteine levels) & restriction of methionine. methionine cycle.

54
Q

vitamin K is involved in..

A

post-translational conversion of glutamate to gamma-carboxyglutamic acid. modification needed for many clotting factors & regulatory proteins in coagulation cascade.

55
Q

common causes of sciata

A

vertebral disc herniation, spinal canal stenosis, irritation by bone spurs, irritation by piriformis (L4-S3, but most commonly involves L5 or S1)

56
Q

transection of sciatic nerve would result in..

A

inability to flex leg at knee, paralysis of muscles below knee

57
Q

differentiate sciatica involving L5 or S1 root

A

compression of L5 –> posterior and lateral thigh and leg pain shooting to inner foot. compression of S1 –> pain strictly in (1) posterior thigh and (2) leg shooting to the foot ACCOMPANIED by weakness of (3) plantar flexion and (4) loss of ankle jerk

58
Q

lateral femoral cutaneous n.

A

L2 and L3, purely sensory n. enters thigh deep to inguinal ligament, supplies most of the skin of anterior thigh

59
Q

L4 damage

A

impaired knee jerk

60
Q

elastin assembly

A

closely related to collagen – synthesized as large polypeptide precusor of 700 amino acids (tropoelastin). primary composed of NON-polar amino acids (glycine, alanine, and valine). like collagen, has proline and lysine. unlike collagen, few of them are hydroxylated. tropoelastin secreted into extracellular space & interact w/ fibrillin. side chains of some lysine residues are covalently bound to form desmosine crosslink.

61
Q

how are elastin and collagen similar (1) ? how do they differ (3)

A

elastin and collagen are both composed of a large number of nonpolar (i.e. lysine/proline) amino acids. differ: (1) in elastin, very few proline and lysine residues are hydroxylated (2) whereas triple helix formation is the basis of the collagen molecule, elastin does not form triple helices (3) triple helix formation in collagen is initiated by hydroxylation, glycosylation, and interchain disulfide bridges at the C-terminus of procollagen molecule. these modifications do not occur in formation of elastin molecules

62
Q

what accounts for elastin’s resilient properties?

A

unique form of desmosine interchain crosslinking between 4 diff lysine residues on 4 diff elastin chains. accomplished by extracellular lysyl hydroxlase

63
Q

anaerobic flora associated w/ aspiration pnemonia (4)

A

bacteriodes, prevotella, fusobacterium, peptostreptococcus

64
Q

lung abscess in aspiration pnemonia usu associated w.

A

usu associated w. polymicrobial infection involving anaerobes (though klebsiella is a common pathogen in alcoholics w/ aspiration pneumonia & can cause monomicrobial lung abscesses)

65
Q

ciprofloxacin and cefazolin’s anaerobe coverage

A

POOR!

66
Q

clindamycin

A

good anaerobe coverage above the belt, also covers aerobic gram positives like s. pneumonia (good for polymicrobial aspiration pneumonia)

67
Q

where does estradiol and progesterone come from in 1st trimester? 2nd & third?

A

1st trimester: corpus luteum. 2nd & 3rd: progesterone -> placenta. estradiol -> fetal adrenal gland (w/ plaecnta.

68
Q

why doesn’t lactation begin in pregnancy?

A

despite high levels of prolactin as pregnancy progresses, high levels of estrogen and progesterone block lactogenesis.

69
Q

hCG

A

secreted by embryonic syncytiotrophoblast during 1st trimester, rising to highest levels at gestational week 9. mid-pregnancy, corpus luteum degenerates and hCG levels fall.

70
Q

4 mature defenses

A

SASH: sublimation (channeling impulses into socially acceptable behaviours), altruism (avoiding negative feelings by helping others), suppression (putting unwanted feelings aside to cope w/ reality), humor (using humor to avoid uncomfortable feelings)

71
Q

cause of monocular scotoma [2]

A

macular degeneration, optic neuritis

72
Q

anopia (loss of vision in 1 eye) [2 causes]

A

(1) retinal artery occlusion (2) central retinal vein occlusion

73
Q

bitemporal hemianopia [3 causes]

A

(1) pressure by pituitary tumor, (2) craniopharyngioma, (3) aneursym of AComm

74
Q

nasal hemianopia (unilateral perichiasmal) [2 causes]

A

(1) calcification or (2) aneursym of internal carotid artery, impinging on uncrossed lateral retinal fibers

75
Q

left homonymous hemianopia [2 causes]

A

optic tract: (1) occlusion of anterior choroidal artery.

optic radiation (2) occlusion of middle cerebral artery branch or (3) lesion involving posterior limb of internal capsule

76
Q

left homonymous superior quadrantanopia (pie in the sky) [1 cause[

A

meyer’s loop in temporal lobe: lesion or stroke in temporal lobe

77
Q

left homonymous inferior quadrantanopia (pie on the floor) [1 cause]

A

dorsal optic radiation: lesion or stroke in parietal lobe

78
Q

left homonymous hemianopia w/ macular sparing [1 cause]

A

occlusion of PCA (macula spared bc collateral blood from MCA)

79
Q

maximum horizontal field of view

A

200 degrees w/ both eyes. central 120 degrees make-up binocular field of view (stereoscopic vision). 2 side fields of 40 degrees seen by only 1 eye (monoscopic vision). note: unilateral visual defects within binocular field of view (i.e. unilateral nasal hemianopia) may be masked due to compensation by normal eye.

80
Q

TT thrombin time prolonged by..? [2]

A

heparin and drugs that directly inhibit thrombin

81
Q

3 rx for DVT

A

(1) vitamin K inhibitors [warfarin] (2) direct factor Xa inhibitors [idraparinux, rivaroxaban, apixaban, fondaparinux – ultralow molecular weight heparin] (3) direct thrombin inhibitors [agratroban, dabigatran (oral)

82
Q

direct factor Xa inhibitors are.. (3). effect on aPTT, PT and TT?

A

indraparinux, rivaroxaban, apixaban ultra low molecular weight heparin. prolong aPTT, PT, but not TT. specific against Xa w/o significant activity against thrombin

83
Q

direct thrombin inhibitors (2) effect on aPTT and PT and TTT?

A

agratroban and dabigatran (oral). prolong TT w/ less effect on aPTT or PT

84
Q

mechanism of unfractionated heparin (2)

A

binds to ATIII and potentiates its action to bind to factor Xa (mainly prolongs aPTT). heparin-antithromin III complex also binds to thrombin and prolongs TT.

85
Q

impetigo-atopic dermatitis is often..

A

superinfected by strep and staph

86
Q

PSGN

A

lumpy-bumpy IF, humps on electron microscopy

87
Q

pituitary apoplexy

A

acute bleeding into a preexisting pituitary adenoma. medical emergency. symptoms are bimodal. acute & chronic. chronic: long-standing symptoms of pituitary tumor (headache, decreasing libido). acute: severe headache, visual disturbances.

88
Q

piuitary apoplexy can mimic..

A

berry aneursym rupture: subarachnoid hemorhhage (bc of signs of meningeal irritation & cranial nerve palsy). differentiate w/ bitemporal hemianopsia (only present in sellar mass w/ suprasellar extension)

89
Q

why does pituitary apoplexy develop into cardiovascular collapse? rx?

A

ACTH deficiency leads to adrenocortical insufficiency. urgent neurosurgical consultation & rx w/ glucocorticoids

90
Q

ischemic necrosis of pituitary

A

sheehan syndrome, typically affects postpartum women. present indolent w/ failure to lactate. acute headache and visual field defects do not occur.

91
Q

compare & contrast unfractionated heparin and LMWH

A

both contain pentasaccharide sequence that binds to (1) antithrombin & causes conformational change that increases ability to inactivate factor Xa. ONLY unfractionated heparin has a pentasaccharide chain long enough >18 saccharide units) to bind both thrombin and antithrombin (together –> ternary complex)

unfractionated heparin has equal activity against factor Xa and thrombin. LMWH: greater activity against factor Xa than thrombin.

92
Q

enoxaparin

A

LMWH. fewer long saccharide units that bind to thrombin. less antithrombotic activity compared to unfractionated heparin

93
Q

fondaparinux

A

synthetic pentasaccharide factor Xa inhibitor. no long saccharide units to bind to thrombin & much lower antithrombin activity compared to unfractionated heparin.

94
Q

areas of necrosis & diminished blood supply (chronic non-healing ulcers) facilitate growth of..

A

anaerobes, like bacteroides

95
Q

piperacillin + tazobactam coverage

A

effective against a large number of gram + and gram - and anaerobic bacteria (including pseudomonas and bacteroides frag)

96
Q

ciprofloxacin is not effective against.. is effective for..

A

ineffective for anaerobic infections. is effective for gram - robs & bacilli, including legionella and p. aeruginosa

97
Q

ceftriaxone is not effective for.. is effective for..

A

ineffective for anaerobes and LAME (listeria, anaerobes, mycoplasma, enterobacter). effective for gram - bacilli, including most enteric organisms: H. flu, Neisseria, Serratia

98
Q

azithromycin use

A

chlamydia, mycoplasma, h. flu, moraxella

99
Q

how is inorganic iodide taken up by thyroid follicular cells? what 3 other things can be taken up by this mechanism?

A

energy-dependent sodium iodide symporter (NIS). also take up (1) perchlorate, (2) pertechnetate, & (3) radioactive iodine. so these can inhibit uptake of one another.

100
Q

rx: exposure to radioactive isotopes of iodine?

A

potassium iodide (KI). competitive inhibition, less radioactive material will be taken up

101
Q

differentiate cGMP sstem from cAMP system

A

cGMP: receptor and guanylate cyclase part of same protein.
cAMP: consists of 4 distinct proteins

102
Q

how does ANP, NO, and sildenafil increase cGMP?

A

ANP: transmembrane receptor/guanylate cyclase complex. NO: cytosolic receptor/guanylate cyclase complex. sildenafil: PDE inhibitor for cGMP

103
Q

signal transduction of vitamin D (1,25-dihydroxycholecalciferol)

A

freely crosses cell membranes and binds to cytosolic receptors. vitamin-receptor complex then crosses nuclear membrane to modify DNA transcription

104
Q

role of carbonic anhydrase in eye

A

carbonic anhydrates modulates HCO3- formation in aqueous humor. inhibition will decrease formation of aqueous humor.

105
Q

common side effects of carbonic anhydrase inhibitors (acetazolamide)? rare?

A

common: somnolence, paresthesias, urine alkalinization. rare: metabolic acidosis, dehydration, hypokalemia, hyponatremia

106
Q

when is disclosure of patient information allowed w/o consent? [4]

A
  1. suspected child / elder abuse
  2. gunshot or stabbing injuries
  3. diagnosis of a reportable communicable disease
  4. pt threatens to physically harm self or others & have reasonable ability to carry out the threat in the future
107
Q

current law on disclosure of paternity to father?

A

a father has no legal right to know if a child is his unless he is ordered to make payments to support that child.

108
Q

theophylline (methylxanthine) mechanism

A

(1) inhibiting phosphodiesterase (increased cAMP). blocks adenosine. results in bronchodilation. cardiotoxic and neurotoxic, narrow TI

109
Q

low-moderate doses of methylxanthine? acute intoxication?

A

low-moderate: mild cortical arousal / insomnia (like caffeine). acute intoxication: GI= abdominal pain, vomiting, diarrhea, TACHYARRYTHMIA, SEIZURE (major cause of morbidity and mortality).

110
Q

rx for theophyllin (methylxanthine) intoxication?

A

rx for intoxication: gastric lavage, administration of activated charcoal (to reduce absorption) and cathartic (increase elimination via GI tract). beta-blockers for tachyarrhythmia. seizures are difficult to treat, but benzo and barbituates.

111
Q

iron poisoning presentation

A

hematemesis and melena (directly toxic to gastric mucosal cells)

112
Q

acetaminophen toxicity? rx?

A

liver damage following a latent period. rx: n-acetyl cysteine (glutathione donor) used in rx of acetaminophen toxicity.

113
Q

nitrites cause cyanosis bc..

A

oxidize ferrous Fe2+ to ferric Fe3+ in heme = methemoglobin

114
Q

methemoglobin

A

oxidation of ferrous Fe2+ to ferric Fe3+ in heme. cannot bind oxygen. cyanosis! fxnl anemia

115
Q

afferent fibers from carotid sinus stretch receptors? aortic arch? where to these afferent fibers terminate?

A

carotid sinus: CN IX, glossopharyngeal (hering’s nerve branch). aortic arch: CN X, vagus. both afferents terminate in solitary nucleus of the medulla

116
Q

penicillinase-stable penicillins

A

oxacillin, nafcillin, methicillin (MRSA is resistant to all three via alterations in penicillin-binding proteins, esp PB2a)

117
Q

cystic hygroma

A

tumors (cystic spaces separated by connective tissue rich in lymphoid aggregates). most commonly located on neck (esp posterior triangle) apparent at birth. often seen in infants w/ turners. results from abnormalities in lymphatic outflow

118
Q

abnormalities in lymphatic outflow in Turner’s results in…

A

cystic hygroma and lymphedema

119
Q

characterestic Turner appearance

A

webbed neck, low hairline, shield chest, short fourth metacarpal, short stature. primary amenorrhea (streak ovaries). failure of secondary sex characteristics. aortic coarct

120
Q

cri du chat presentation

A

5p- : round face, cat-like cry, microcephaly

121
Q

down’s face

A

flat face, oblique palpebral fissues, epicanthal folds

122
Q

testicular feminization syndrome (androgen insensitivty syndrome)

A

defect in testosterone receptors. karyotype 46 XY phenotypically normal females (but, blind ended vaginal pouch w/o uterus). will have testes (determined by presence of SRY on Y chromosome) and regression of female internal organs bc of sertoli cells (anti-mullerian hormone) –> no uterus and fallopian tubes.

123
Q

3 classes of alzeheimer’s drugs

A

(1) enhanced cholinergic neurotransmission [donezpil - AchE] (2) neuroprotection via antioxidants [vitamin E – alpha-tocopherol] (3) NMDA receptor antagonism [memantine]

124
Q

lecithin-sphinomyelin ratio

A

marker of fetal lung maturity. mature = above 1.9. determined by outward flow of pulmonary secretions from fetal lungs into amniotic fluid. lecithin-sphinomyelin ratio is equal until 32-33 wks gestation, when lecithin conc increase significantly while sphingomyelin stays same.

125
Q

which maternal fluid has greatest effect on lecithin-sphingomyelin ratio? what others paly a role?

A

GLUCOCORTICOIDS (biggest role). also prolactin, insulin, estrogens, androgens, thyroid hormones, and catecholamines.

126
Q

fetal adrenal gland

A

inner active fetal zone, outer dormant adult zone. fetal zone = androgens in concert w/ placenta (lacks 3-beta-hydroxysteroid dehydrogenase needed to convert pregnenolone to progesterone). outer = dormant but makes some cortisol, gradually increases later in gestation

127
Q

cortisol needed for fetal lung maturation from..?

A

BOTH maternal and fetal cortisol. outer adult zone of fetal adrenal gland. dormant in early fetal life, but produces cortisol later in gestation. controlled by ACTH and CRH from both (1) fetal pituitary and (2) placenta. positive feedback: CRH secretion from placenta upregulated by cortisol.

128
Q

oxytocin levels through pregnancy

A

stimulate myometrial contraction. oxytocin levels mostly constant during gestation. but increased expression of oxytocin RECEPTORS in myometrium later in gestation (increased sensitivity)

129
Q

transition from in situ tumor to metastatic disease defined by ability of tumor cells to invade local tissue and cross tissue barriers. 3 steps.

A
  1. detachment: decreased expression of adhesion molecules (often E-cadherins). 2. adhere to basement membrane: often via laminin expression.
  2. invasion of the basement membrane: secretion of proteolytic enzymes by tumor cells: metalloproteases & cathepsin D protease
130
Q

encapsulation

A

when a tumor pushes against, but does not invade fibrous tissue (meningiomas can do this)

131
Q

metalloproteases contain..

A

zinc

132
Q

pulmonary venous HTN produces which 3 sequential things?

A

(1) pulmonary interstitial edema in interlobular septa (2) edematous widening of alveolar septa (3) intra-alveolar accumulation of edema fluid.

133
Q

orthopnea (supine dyspnea relieved by sitting) is caused by…

A

SPECIFIC sign of advanced LEFT HEART failure (can also occur w. mitral stenosis –> acute exacerbation of baseline pulmonary edema when central venous, pulmonary venous, cardiac filling pressures are increased due to redistribution of blood that had been pooled in veins when standing back into central circulation. ca==

134
Q

cardiac asthma

A

wheezing on exertion resulting from left heart failure. due to increased venous return to heart w/ exercise, but poor left ventricle fxn.

135
Q

wheezing on exertion caused by which 3 things?

A

(1) cardiac asthma (2) asthma (3) chronic obstructive pulmonary disease

136
Q

pink frothy sputum

A

in patients w/ left ventricle failure (or other causes of pulmonary edema) due to ruption of bronchial veins.