test #19 4.9 Flashcards Preview

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Flashcards in test #19 4.9 Deck (97)
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1
Q
osteocytes (trapped osteoblasts) are connected to one another via..
A
cytoplasmic extension travel from lacunae through canaliculi, connect via GAP JUNCTION. send signals & exchange nutrients & waste products
2
Q
tight junctions
A
zona occludens (1st component of junctional compelx)
3
Q
intermediate junctions
A
zona adherens (2nd component of junctional complex)
4
Q
desmosomes
A
3rd component of junctional complex
5
Q
maternal blood types A and B often have what type of anti-B and anti-A Abs (respectively)? what about type O?
A
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
Q
in what maternal blood type do we worry about erythroblastosis fetalis and hemolytic disease of newborn?
A
type O moms with type B or A babies. bc they make anti-B or A IgG.
7
Q
common carotids from what aortic arch?
A
3rd
8
Q
1st branchial/pharyngeal arch? associated w/ which n.
A
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
Q
embryological origin of branchial arches (2)
A
muscle & arteries = mesoderm.

bone = neural crest cells
10
Q
2nd branchial/pharyngeal arch? associated n?
A
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
Q
4th and 6th arch
A
make up cartilaginous structures of larynx.
12
Q
3 most common causes of metabolic alkalosis
A
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
Q
bilateral lesions in mamillary bodies & periaqueductal grey area in hospital (in alcoholic)
A
due to glucose infusion w/o thiamine in thiamine deficient person. PDH needs thiamine!
14
Q
wernicke encephalopathy
A
(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
Q
infuse glucose + ___ in alcoholics & bad diet
A
THIAMINE (B1)
16
Q
heterophile negative mononucleosis (3)?
A
CMV, HHV-6, toxoplasmosis
17
Q
coxsackie A causes (2)
A
(1) asceptic meningitis and (2) herpangina in children
18
Q
nifedipine can..
A
elevate capillary hydrostatic pressure --> edema
19
Q
common causes of lymphatic obstruction (3)
A
(1) filariasis,(2) invasive malignancy, (3) iatrogenic (surgical lymph node dissection & radiation therapy)
20
Q
downstream signaling targets of insulin
A
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
Q
facial n. constituents.. (4)
A
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
Q
geniculate ganglion
A
parasympathetic ganglion for submandibular, sublingual, and lacrimal glands. innervated by facial n.
23
Q
motor in trigeminal?
A
V3 -- muscles of mastication and tensor tympani
24
Q
filtration fraction
A
fraction of PLASMA entering the kidney that filters into renal tubular lumen.

FF = GFR/(1-Hct x RBF)
25
Q
in gastrectomy, must supplement with
A
B12 (water soluble vitamin)
26
Q
role of pepsin in digestion
A
activated by HCl, cleaves polypeptides at sites of aromatic amino acids. helpful, but not required for protein digestion.
27
Q
premature ovarian failure age? mean age of menopause in US? marker?
A
ovarial failure before 35. mean age of menopause in US: 52. HIGH FSH (above 30uL)
28
Q
urinary 17-ketosteroids
A
measure adrenal androgens (DHEA, DHEA-S, 4androstenedione)
29
Q
chronic lymphedema is a risk factor for..
A
development of cutaneous angiosarcoma (St
30
Q
chronic lymphedema is a risk factor for..
A
cutaneous (lymph)angiosarcoma.

classic: radical masectomy w/ axillary lymph node dissection --> multiple firm violaceous nodules
31
Q
prognosis of angiosarcoma?
A
POOR, tumor usu wide spread by diagnosis.
32
Q
histopathology of angiosarcoma
A
infiltration of dermis w/ slit-like abnormal vascular spaces
33
Q
breast cancer is most likely to metastasize to..
A
bone, liver, lung
34
Q
stewart-treves syndrome
A
chronic lymphedema ---> angiosarcoma
35
Q
presentation of hepatitis A virus
A
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
Q
infection involving central venous catheters are often originate from...
A
patient's skin flora OR bacteria on hands of HCW

(gram positive cocci -- coag neg staph & staph aureus)
37
Q
steps to reduce CVC infxn? what's not needed?
A
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
Q
process of type I collagen synthesis
A
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
Q
two possible enzyme deficiences in Ehlers-Danlos
A
(1) lysyl-hydroxlase: hydroxylate single chain.
(2) procollagen peptidase: cleave terminal chains extracellularly, allowing for tropocollagen full helix formation.
40
Q
distinguishing Ehlers-Danlos due to (1) lysyl hydroxylase deficience or (2) propeptidase deficiency
A
(1) lysyl hydroxylase: kyphoscoliosis & ocular fragility: have less hydroxylysine in collagenous tissue.

(2) procollagen peptidase: disulfide-rich globular domain.
41
Q
choroid plexus in which ventricles
A
lateral & 4th
42
Q
causes of congenital noncommunicating hydrocephalous (3)
A
aqueductal stenosis, arnold-chiari, dandy-walker
43
Q
high NADH w/ low glucose?
A
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
Q
causes of lactic acidosis
A
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
Q
most dependent regions of lung in supine individual (2) i.e. sites for aspiration when laying down?
A
(1) superior regions of lower lobes.
(2) posterior regions of upper lobes.
46
Q
culprits in aspiration pnemonia?
A
anaerobics inhabitants of upper airway: peptostreptococcus, bacteroides, prevotella, fusobacterium.
47
Q
4 loop diuretics
A
furosemide, torsemide, bumetanide, ethacrynic acid (greatest risk of ototoxicity)
48
Q
triamterene & amiloride
A
blocks ENac.
49
Q
common ototoxic agents?
A
aminoglycosides, salicylates, cisplatin
50
Q
busipirone
A
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
Q
anti-anxiety rx in patient w/ history of benzo abuse
A
busipirone! low abuse potential.
52
Q
acutely injured child, suspected child abuse. first thing done?
A
call child protective services: DOCUMENT & get social work involved.

have THEM evaluate / intervene w/ parents and see what's up.
53
Q
best auscultory indicator of mitral stenosis severity? why?
A
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
Q
cladribine? rx for?
A
purine analog, resistant to degradation by adenosine deaminase. urx for hairy cell leukemia.
55
Q
cyclophosphamide
A
alklyating agent & cross-link, must be activated by P450.
56
Q
lomustine
A
nitrosurea. good CNS penetration. alkylating agent & crossbridge. nonenzymatic hydroxlation to be active.
57
Q
dacarbazine
A
cell-cycle nonspecific methylating agent. requires enzymatic activation
58
Q
cisplatin. prevent nephrotoxicity w/?
A
platinum-containing chemotherapeutic. hydrated to be cytotoxic. prevent nephrotoxicity w/ amofostine (free radical scavenger) and Cl- diuresis.
59
Q
methotrexate
A
folic acid analogue, inhibits dihydrofolate reductase.
60
Q
mercaptopurine
A
purine analogue. activated by HGPRT (guanine --> GMP and hypoxanthine --> IMP) and metabolised by xanthine oxidase. (toxicity increases w/ allopurinol)
61
Q
3 clases of antimetabolites?
A
(1) folate antagonist (2) purine analogue (3) pyrmidine analogue
62
Q
rx for absence seizures
A
ethosuximide & valproate
63
Q
tonic clonic & absence seizures
A
valproate works on both
64
Q
ethosuximide works by..
A
blocking thalamic Ca2+ channels
65
Q
drug of choice for complex partial seizure? feared side effects?
A
carbamazepine: fear agranulocytosis and aplastic anemia7h
66
Q
why do opiods cause constipation? miosis?
A
bind to mu-opioid receptors in GI tract, cause decreased secretions and gastric motility. miosis-- activation of parasympathetics
67
Q
most common and unpleasant side effect of opiod use?
A
nausea. stimulate chemoreceptor trigger zone leading to emesis. tolerance will develop
68
Q
how do thiazides (chlorthiadone, hydrochlorothiazide) cause hypercalcemia?
A
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
Q
thiazide and thiazide-like diuretics
A
chlorthiadone, hydrochlorothiazide, indapamide, metolazone (diff potency, bioavailability, half-life)
70
Q
C. diff toxin affects
A
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
Q
drugs associated w/ mitochondrial toxicity?
A
cyanide, nucleoside reverse transcriptase inhibitors (nRTIS
72
Q
lecithinase alpha toxin released by?
A
C. perfringens. watery diarrhea, gas gangrene.
73
Q
how does antagonism of muscarinic lead to flushed cheeks?
A
inhibition of eccrine sweat glands --> fever ---> compensatory cutaneous vasodilation.
74
Q
diphenhydramine? side effects?
A
H1-receptor antagonist, has ANTI-CHOLINERGIC effects
75
Q
H1 receptors cause..
A
vascular permeability and bronchoconstriction
76
Q
5 drugs w/ antimuscarinic effects
A
atropine, TCA's (amitriptyline), H1 receptor antagonist (diphenhydramide) neuroleptics, antiparkinsonian drugs
77
Q
venous drainage from lower limb
A
from superficial veins through perforating veins into deep veins of extremities. deep veins --> inferior vena cava.

incompentence of venous valves : varicose veins
78
Q
stasis dermatitis
A
chronic venous insufficency (i.e. from varicose veins can lead to) ---> erythema and scaling w/ progressive dermal fibrosis & hyperpigmentation
79
Q
paroxysmal nocturnal hemoglobinura presents with.. (3). explain misnomer.
A
(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
Q
pathophysiology in PNH (paroxysmal nocturnal hemoglobinuria)
A
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
Q
deficiency of CD55 and CD59
A
PAROXYSMAL NOCTURNAL HEMOGLOBINURIA. normally. inactivate complement on RBCs. not expressed on surface in PNH.
82
Q
achondroplasia inheritance
A
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
Q
PCOS pathophysiology
A
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
Q
rx for PCOS (stein-leventhal syndrome)
A
clomiphene: SERM; prevents negative feedback inhibition on hypothalamus by circulating estrogen. increases FSH and LH --> ovulation
85
Q
unopposed elevated estrogen in PCOS increases risk for...? specific rx for this?
A
endometrial hyperplasia --> endometrial carcinoma. rx: progesterone!
86
Q
clomiphene
A
SERM. prevents negative feedback inhibition on hypothalamus by circulating estrogens. (increase FSH and LH). for ovulation.
87
Q
why are lower lung fields most affected by panacinar emphysema?
A
more perfusion, greater neutrophil invasion, more elastase.
88
Q
coffee ground emesis
A
blood in vomitus that has been exposed to gastric acid. (colour from oxidation of heme iron).
89
Q
body can sustain normal BP and CO with how much blood loss? what occurs when more is lost?
A
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
Q
most important intervention in hypovolemic shock>
A
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
Q
passive-aggressive
A
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
Q
acting out
A
immature defense that involves expressing unconscious wishes or impulses through actions. i.e. temper tantrum
93
Q
isolation
A
coping mechanism, separation of an idea and its accompanying emotions. i.e. discussing war in nonemotional terms
94
Q
undoing
A
symbolically nullifying an unacceptable or guilt-proviking throught, idea, feeling, by confession / atonement.
95
Q
extensive cerebellar purkinje cell degeneration w/ lung cancer?
A
immune-mediated paraneoplastic cerebellar degeneration. associated w/ lung, breast, ovary, uterus, lymphoma cancer.
96
Q
antibodies associated with paraneoplastic cerebellar degeneration
A
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
Q
paraneoplastic
A
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]