test #19 4.9 Flashcards Preview

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Flashcards in test #19 4.9 Deck (97):
1

osteocytes (trapped osteoblasts) are connected to one another via..

cytoplasmic extension travel from lacunae through canaliculi, connect via GAP JUNCTION. send signals & exchange nutrients & waste products

2

tight junctions

zona occludens (1st component of junctional compelx)

3

intermediate junctions

zona adherens (2nd component of junctional complex)

4

desmosomes

3rd component of junctional complex

5

maternal blood types A and B often have what type of anti-B and anti-A Abs (respectively)? what about type O?

A and B have IgM (doesn't cross placenta).

type O have predominately IgG anti-A and anti-B type (can cross placenta & cause hemolytic disease of newborn in 3% of pregnancies). can happen w/ 1st pregnancy.

6

in what maternal blood type do we worry about erythroblastosis fetalis and hemolytic disease of newborn?

type O moms with type B or A babies. bc they make anti-B or A IgG.

7

common carotids from what aortic arch?

3rd

8

1st branchial/pharyngeal arch? associated w/ which n.

associated w/ trigeminal n.

neural crest cells make: Maxilla, zygoma, Mandible, vomer, palatine, incus, Malleus. (M's)

mesoderm: muscles of mastication (temporalis, medial / lateral pterygoid, masseter) anterior belly of digastric, mylohyoid, tensor tympani, tensor veli palatini.

9

embryological origin of branchial arches (2)

muscle & arteries = mesoderm.

bone = neural crest cells

10

2nd branchial/pharyngeal arch? associated n?

associated w/ facial n.

neural crest: styloid process, lesser horn of hyoid, stapes.

mesodern: muscles of facial expression, stylohyoid, stapedius, posterior belly of digastric

11

4th and 6th arch

make up cartilaginous structures of larynx.

12

3 most common causes of metabolic alkalosis

1. LOSS OF H+ from body: vomiting, nasogastric suction. loose HCl in gastric secretion, causes serum Cl- to decrease

(leads to DECREASED urinary Cl-, t help. SALINE-RESISTANT

13

bilateral lesions in mamillary bodies & periaqueductal grey area in hospital (in alcoholic)

due to glucose infusion w/o thiamine in thiamine deficient person. PDH needs thiamine!

14

wernicke encephalopathy

(1) opthalmoplegia: horizontal nystagmus, bilateral abducens palsy, complete opthalmoplegia
(2) ataxia: degeneration of all layers of cortex
(3) confusion, apathy, inattentiveness, disorientation: from encephalopathy.

characterestic hemorrhage into mamillary body

15

infuse glucose + ___ in alcoholics & bad diet

THIAMINE (B1)

16

heterophile negative mononucleosis (3)?

CMV, HHV-6, toxoplasmosis

17

coxsackie A causes (2)

(1) asceptic meningitis and (2) herpangina in children

18

nifedipine can..

elevate capillary hydrostatic pressure --> edema

19

common causes of lymphatic obstruction (3)

(1) filariasis,(2) invasive malignancy, (3) iatrogenic (surgical lymph node dissection & radiation therapy)

20

downstream signaling targets of insulin

generally: insulin receptor substrates (IRS), leading to acrivation of a PROTEIN PHOSPHATASE.

DEPHOSPHORYLATES GLYCOGEN SYNTHASE (1. activates glycogen synthase to promote glycogen synthesis & 2. dephosphorylates fructose 1,6 bisphosphatase to inactivate & block gluconeogenesis)

21

facial n. constituents.. (4)

1. motor to facial muscles
2. parasympathetic to lacrimal, submandibular, sublingual salivary glands.
3. special afferent fibers for taste (ant 2/3)
4. somatic afferents from pinna and external auditory canal

bell's palsy: unilateral face paralysis (impaired eye closure, eyebrow sagging, inability to smile/frown on affected side, loss of nasolabial fold, mouth drawn to non-affected side. can have: decreased tearing, hyperacusis, loss of taste sensation over anterior 2/3rd of tongue

22

geniculate ganglion

parasympathetic ganglion for submandibular, sublingual, and lacrimal glands. innervated by facial n.

23

motor in trigeminal?

V3 -- muscles of mastication and tensor tympani

24

filtration fraction

fraction of PLASMA entering the kidney that filters into renal tubular lumen.

FF = GFR/(1-Hct x RBF)

25

in gastrectomy, must supplement with

B12 (water soluble vitamin)

26

role of pepsin in digestion

activated by HCl, cleaves polypeptides at sites of aromatic amino acids. helpful, but not required for protein digestion.

27

premature ovarian failure age? mean age of menopause in US? marker?

ovarial failure before 35. mean age of menopause in US: 52. HIGH FSH (above 30uL)

28

urinary 17-ketosteroids

measure adrenal androgens (DHEA, DHEA-S, 4androstenedione)

29

chronic lymphedema is a risk factor for..

development of cutaneous angiosarcoma (St

30

chronic lymphedema is a risk factor for..

cutaneous (lymph)angiosarcoma.

classic: radical masectomy w/ axillary lymph node dissection --> multiple firm violaceous nodules

31

prognosis of angiosarcoma?

POOR, tumor usu wide spread by diagnosis.

32

histopathology of angiosarcoma

infiltration of dermis w/ slit-like abnormal vascular spaces

33

breast cancer is most likely to metastasize to..

bone, liver, lung

34

stewart-treves syndrome

chronic lymphedema ---> angiosarcoma

35

presentation of hepatitis A virus

most often silent "anicteric". sometimes: acute, self-limited illness characterized by jaundice, malaise, fatigue, anorexia, N/V, RUQ pain, or AVERSION TO SMOKING.

infxn usu more severe in adults

36

infection involving central venous catheters are often originate from...

patient's skin flora OR bacteria on hands of HCW

(gram positive cocci -- coag neg staph & staph aureus)

37

steps to reduce CVC infxn? what's not needed?

most important: hand hygiene -- washing & gloves. chlorhexidine for skin disinfection, avoid femoral insertion site. remove when no longer needed.

NOT NEEDED: TOPICAL antibiotics not needed (increase resistance & candida prolif), ORAL antibio, routine replacement.

38

process of type I collagen synthesis

in ER:
(1) HYDROXYLATE select pro & lys residue [vit C dep]
(2) GLYCOSYLATE select lys residue w/ galactose & glucose
(3) assemble into procollagen TRIPLE helix
golgi --> secreted

outside:
(1) terminal propeptides (INTRAchain disulfides) cleaved N- and C- procollagen peptidases ---> TROPOCOLLAGEN.
(2) collagen fibrils spontaneously assemble
(3) LYSYL OXIDASE (Cu2+) covalently cross-links

39

two possible enzyme deficiences in Ehlers-Danlos

(1) lysyl-hydroxlase: hydroxylate single chain.
(2) procollagen peptidase: cleave terminal chains extracellularly, allowing for tropocollagen full helix formation.

40

distinguishing Ehlers-Danlos due to (1) lysyl hydroxylase deficience or (2) propeptidase deficiency

(1) lysyl hydroxylase: kyphoscoliosis & ocular fragility: have less hydroxylysine in collagenous tissue.

(2) procollagen peptidase: disulfide-rich globular domain.

41

choroid plexus in which ventricles

lateral & 4th

42

causes of congenital noncommunicating hydrocephalous (3)

aqueductal stenosis, arnold-chiari, dandy-walker

43

high NADH w/ low glucose?

suggests another fuel is being used by body. i.e. ethanol.

ethanol --> acetaldehyde --> acetate. produces 2 NADH.

high NADH/NAD+ ratio. promotes pyruvate to lactate, oxaloacetate to malate. inhibits gluconeogenesis. HYPOGLYCEMIA.

44

causes of lactic acidosis

1. enhanced metabolic rate (seizure/exercise)
2. reduced oxygen delivery (cardiac/pulmonary failure, shock, tissue infarction --> decreased oxidative phosphorylation.
3. diminished lactate catabolism (hepatic failure or hypoperfusion.
4. decreased oxygen utilization (cyanide posioning)
5. enzymatic defects in glycogenolysis / gluconeogenesis

45

most dependent regions of lung in supine individual (2) i.e. sites for aspiration when laying down?

(1) superior regions of lower lobes.
(2) posterior regions of upper lobes.

46

culprits in aspiration pnemonia?

anaerobics inhabitants of upper airway: peptostreptococcus, bacteroides, prevotella, fusobacterium.

47

4 loop diuretics

furosemide, torsemide, bumetanide, ethacrynic acid (greatest risk of ototoxicity)

48

triamterene & amiloride

blocks ENac.

49

common ototoxic agents?

aminoglycosides, salicylates, cisplatin

50

busipirone

5-HT1A agonist w/ minimal hypnotic, sedative, euphoric, muscle relaxant effects.

good for GENERALIZED anxiety disorder. not for more specific ones.

low abuse potential

51

anti-anxiety rx in patient w/ history of benzo abuse

busipirone! low abuse potential.

52

acutely injured child, suspected child abuse. first thing done?

call child protective services: DOCUMENT & get social work involved.

have THEM evaluate / intervene w/ parents and see what's up.

53

best auscultory indicator of mitral stenosis severity? why?

S2-to-OS time. shorter interval, more SEVERE stenosis.

OS: tensing of mitral valve leaflets after cusps have completed opening. (1) more thickened/fibrotic --> earlier tensing.

also, A2-OS interval inversely correlates w/ (2) left atrial pressure.

54

cladribine? rx for?

purine analog, resistant to degradation by adenosine deaminase. urx for hairy cell leukemia.

55

cyclophosphamide

alklyating agent & cross-link, must be activated by P450.

56

lomustine

nitrosurea. good CNS penetration. alkylating agent & crossbridge. nonenzymatic hydroxlation to be active.

57

dacarbazine

cell-cycle nonspecific methylating agent. requires enzymatic activation

58

cisplatin. prevent nephrotoxicity w/?

platinum-containing chemotherapeutic. hydrated to be cytotoxic. prevent nephrotoxicity w/ amofostine (free radical scavenger) and Cl- diuresis.

59

methotrexate

folic acid analogue, inhibits dihydrofolate reductase.

60

mercaptopurine

purine analogue. activated by HGPRT (guanine --> GMP and hypoxanthine --> IMP) and metabolised by xanthine oxidase. (toxicity increases w/ allopurinol)

61

3 clases of antimetabolites?

(1) folate antagonist (2) purine analogue (3) pyrmidine analogue

62

rx for absence seizures

ethosuximide & valproate

63

tonic clonic & absence seizures

valproate works on both

64

ethosuximide works by..

blocking thalamic Ca2+ channels

65

drug of choice for complex partial seizure? feared side effects?

carbamazepine: fear agranulocytosis and aplastic anemia7h

66

why do opiods cause constipation? miosis?

bind to mu-opioid receptors in GI tract, cause decreased secretions and gastric motility. miosis-- activation of parasympathetics

67

most common and unpleasant side effect of opiod use?

nausea. stimulate chemoreceptor trigger zone leading to emesis. tolerance will develop

68

how do thiazides (chlorthiadone, hydrochlorothiazide) cause hypercalcemia?

block Na+ Cl- symporter apically. less intracellular Na+. stimulates basolateral Na+/Ca2+ exchanger, bring more Na+ in, Ca2+ out.

less intracellular Ca2+ --> more luminal Ca2+ absorption in DCT. also, increase Ca2+ in PCT due to volume depletion may occur.

69

thiazide and thiazide-like diuretics

chlorthiadone, hydrochlorothiazide, indapamide, metolazone (diff potency, bioavailability, half-life)

70

C. diff toxin affects

toxin A and B, both internalized.

toxin A: neutrophil chemoattractant, mucosal inflammation loss of water into gut mucosa, results in mucosal death.

toxin B: actin depolymerization, loss of cellular cytokeleton, death and necrosis

71

drugs associated w/ mitochondrial toxicity?

cyanide, nucleoside reverse transcriptase inhibitors (nRTIS

72

lecithinase alpha toxin released by?

C. perfringens. watery diarrhea, gas gangrene.

73

how does antagonism of muscarinic lead to flushed cheeks?

inhibition of eccrine sweat glands --> fever ---> compensatory cutaneous vasodilation.

74

diphenhydramine? side effects?

H1-receptor antagonist, has ANTI-CHOLINERGIC effects

75

H1 receptors cause..

vascular permeability and bronchoconstriction

76

5 drugs w/ antimuscarinic effects

atropine, TCA's (amitriptyline), H1 receptor antagonist (diphenhydramide) neuroleptics, antiparkinsonian drugs

77

venous drainage from lower limb

from superficial veins through perforating veins into deep veins of extremities. deep veins --> inferior vena cava.

incompentence of venous valves : varicose veins

78

stasis dermatitis

chronic venous insufficency (i.e. from varicose veins can lead to) ---> erythema and scaling w/ progressive dermal fibrosis & hyperpigmentation

79

paroxysmal nocturnal hemoglobinura presents with.. (3). explain misnomer.

(1) hemolytic anemia (2) hypercoagulable state (3) decreased blood count.

hemolysis only appears to be nocturnal bc urine collects & concentrates overnight, causing dramatic color change in morning. can technically occur all day.

80

pathophysiology in PNH (paroxysmal nocturnal hemoglobinuria)

mutation in PIG-A (codes for GPI-anchor) needed for attachment of CD55 CD59. cell surface markers that inactivate complement. results in hemoylsis and thrombisis (COD)

81

deficiency of CD55 and CD59

PAROXYSMAL NOCTURNAL HEMOGLOBINURIA. normally. inactivate complement on RBCs. not expressed on surface in PNH.

82

achondroplasia inheritance

85% sporadic, associated w/ advanced paternal age. 15% AUTOSOMAL DOMINANT.

if family ask about inheritance, since achondroplasia is relatively rare, the 85% chance of sporadic mutation does not significantly factor into the 50% risk of inheritance (w/ inherited mutation)

83

PCOS pathophysiology

unnknown. persistently elevated estrogen, androgen, and LH.

hyperandrogenism, chronic anovulation, oligomenorrhea, and multiple ovarian cysts.

often have obesity, insulin resistance, and dyslipidemia.

present w/ enlarged ovaries w/ thickened endometrium (risk for endometrial hyperplasia)

84

rx for PCOS (stein-leventhal syndrome)

clomiphene: SERM; prevents negative feedback inhibition on hypothalamus by circulating estrogen. increases FSH and LH --> ovulation

85

unopposed elevated estrogen in PCOS increases risk for...? specific rx for this?

endometrial hyperplasia --> endometrial carcinoma. rx: progesterone!

86

clomiphene

SERM. prevents negative feedback inhibition on hypothalamus by circulating estrogens. (increase FSH and LH). for ovulation.

87

why are lower lung fields most affected by panacinar emphysema?

more perfusion, greater neutrophil invasion, more elastase.

88

coffee ground emesis

blood in vomitus that has been exposed to gastric acid. (colour from oxidation of heme iron).

89

body can sustain normal BP and CO with how much blood loss? what occurs when more is lost?

10%. more than this --> sympathetic nervous system activated: constriction of arteriole & venous beds & stimulation of heart.

constrict arterioles: increase total peripheral resistance, maintain end organ pressure. shunt blood from extremities.

constrict venous: increase blood return to heart, maintain PRELOAD

stimulate heart: increased contractility and HR.

90

most important intervention in hypovolemic shock>

even before identify/eliminate source of bleeding is:

RAPID INFUSION OF BLOOD AND CRYSTALLOID SOLUTION like normal saline. increase intravascular volume & ventricular preload --> increases end-diastolic sarcomere length -- > increased stroke volume and cardiac output

91

passive-aggressive

expressing aggression towards others by passively refusing to meet their needs. i.e. missing appointments. act out hostile feelings in a non-confrontational manner.

92

acting out

immature defense that involves expressing unconscious wishes or impulses through actions. i.e. temper tantrum

93

isolation

coping mechanism, separation of an idea and its accompanying emotions. i.e. discussing war in nonemotional terms

94

undoing

symbolically nullifying an unacceptable or guilt-proviking throught, idea, feeling, by confession / atonement.

95

extensive cerebellar purkinje cell degeneration w/ lung cancer?

immune-mediated paraneoplastic cerebellar degeneration. associated w/ lung, breast, ovary, uterus, lymphoma cancer.

96

antibodies associated with paraneoplastic cerebellar degeneration

anti-yo: ovary/breast.
anti-P/Q: lung
anti-Hu: lung

anti-tumor Ab cross-react w/ neurons, degeneration of cerebellum. present w/ limb / truncal ataxia etc.

97

paraneoplastic

associated w/ systemic cancer, but NOT due to metastasis, metabolic defects, nutritional deficency, infxn, coagulopathy, or side effects of therapy.

associated w/ substances produced by tumor cell (i.e. induction of autoimmune phenomena [cerebellar degeneration], or hormone-like substances [ACTH, PTHrP]