test #41 4.30 Flashcards
(127 cards)
1
Q
immunoglobulins made by Salk polio vaccine?
A
killed – only IgG
injected intramuscularly, unable to stimulate mucosal secretory IgA
2
Q
immunoglobulins made by Sabin polio vaccine?
A
live – both IgG and IgA on (mucosal surfaces)
will colonize natural site of viral entry, producing a greater & more prolonged immune response there.
3
Q
difference between Salk & Sabin’s polio vaccine
A
Salk - killed. less effective in generating prolonged oropharyngeal & intestinal IgA
(not serum)
Sabin - live, will be able to colonize mucosal surface and secrete IgA
4
Q
two primary sites of poliovirus replication
A
oropharynx & intestine
5
Q
common sites of psoriasis
A
elbow, knees, gluteal cleft, lumbosacral area, glans penis, scalp
6
Q
nail changes associated w/ psoriasis
A
yellow-brown discoloration w/ pitting, thickening, or crumbling
7
Q
type of arthritis w/ psoriasis
A
often deforming, upper extremity, small joint
dactylitis (sausage fingers), pencil-in-cup defomity on x-ray
8
Q
HLA subtype associated w/ psoriasis
A
HLA C
HLAB27 too bc of psoriatic arthritis
9
Q
who makes angiotensin converting enzyme?
A
pulmonary vascular endothelial cells
10
Q
three direct effects of antgiotensin II
A
- sodium retention (direct)
- aldosterone production
- vasconstriction
11
Q
negative predictive value.
“what’s the probability that negative test results truly mean absence of disease”
A
of the people who tested negative, how many don’t have the disease
12
Q
relationship of NPV and prevalence
A
NPV decreases as prevalence increases
13
Q
Gardos channel blockers for Sickle-cell anemia
A
Ca2+ dependent K+ channel blockers, reduces K+ & H2O efflux from erythrocytes
prevents dehydration & sickling in Sickle-cell anemia
14
Q
which substances increase gastric acid production from parietal cells? block
A
increase: histamine, Ach, gastrin
block: PGE2
15
Q
predominant source of TGF-alpha
A
CARCIMONAS
also, mac
16
Q
cachexia cytokines
A
TNF-alpha, IFN-gamma, IL-6
17
Q
what can severely impair cardiac output in patients w/ aortic stenosis
A
sudden drop in preload w/ loss of atrial contraction (i.e. atrial fibrillation)
bc left heart needs to generate lots of pressure to get blood out in aortic stenosis, now relies on atrial contraction for maximal preload (max LV filling)
18
Q
in which pts is atrial contraction importrant
A
patients w/ poorly compliant left ventricles. needed to maintain adequate LV filling.
19
Q
definition of preload
A
end-diastolic volume in ventricle
20
Q
definition of afterload
A
arterial resistance
21
Q
where does CN I olfactory bundles enter skull?
A
cribiform plate
22
Q
what goes through optic canal
A
- CN II
- central retinal vein
- opthalmic artery
23
Q
what goes through superior orbital fissure?
A
- CN III
- CN IV
- CN VII
- CN V1
- opthalmic vein
- sympathetic fibers
24
Q
foramen rotundum
A
CN V2
25
foramen ovale
CN V3
26
foramen spinosum
middle meningeal artery & vein
27
internal acoustic meatus
CN VII
| CN VIII
28
jugular foramen
CN IX,
CNX,
CN XI,
jugular vein
29
foramen magnum
spinal root of CN XI
brain stem
vertebral artery
30
hypoglossal canal
CN XII
31
jugular foramen (vernet) syndrome
loss of CN IX, X, XI
- loss of taste from posterior 1/3 tongue (CN IX)
- reduce parotid gland secretion (CN IX)
- loss of gag reflex (CN IX, X)
- dysphagia (CN IX, X)
- dysphonia/hoarseness (CN X)
- soft palate drop w/ deviation of uvula to normal side (CN X)
- SCN and trapezius paralysis (CN XI)
32
air in the gallbladder biliary tree suggests
gallstone ileus
33
where does gallstone lodge in gallstone ileus
trapped behind the ileocecal valve.
see it in ileum
34
choledocolithiasis
obstruction of cystic or common bile duct by gallstone
35
mechanism of genomic imprinting
DNA methylation by DNA methytransferases
transfer methy from donors, like S-adenosyl-methionine (SAM) to CYSTEINE residues
36
describe airway resistance
upper respiratory tract: nasal passage, mouth, pharynx, larynx = 1/2
trachea & mainstem bronchus: HIGH
increases in MEDIUM-sized bronchi bc of highly turbulent flow (generation 2-5)
falls in smaller airways bc high cross-sectional area is combined high.
37
what constitutes "upper" respiratory tract
nasal passage, mouth, pharynx, larynx
38
what constitutes "lower" respiratory tract
trachea & 23 generation of airways
39
where is lower respiratory airway resistance highest
MEDIUM-sized bronchi (generation 2-5) bc of turbulent flow
moderately high in trachea too. falls after medium sized bronchi (bc summation of cross-sectional area = low)
40
antipseudomonal penicillins
ticarcillin, piperacillin
41
antipseudomonal cephalosporins
ceftazidime (3rd gen)
| cefepime (4th gen)
42
antipseudomonal aminoglycosides
amikan, gentamycin, tobramycin
43
antipseudomonal fluroquinolones
ciprofloxacin
| levofloxacin
44
antipseudomonal monobactam
aztreonam
45
antipseudomonal carbapenem
imipenem
| meropenem
46
azetreonam works on
aerobic gram negatives
| bad against gram positive and anerobes
47
what type of haemophilus produces ear infxn
noncapsular, nontypable
h. flu vaccine won't prevent it
48
what kind of illness can nontypable h. flu cause?
part of upper respiratory normal flora
otitis media
sinusitis
bronchitis
49
type of immunity conferred by conjugated vaccine
humoral.
adding protein helps it be presented on MHC II.
doesn't stimulate a cell-mediated response (not on MHC I)
50
time frame for ischemic-related brain injury
hypoxia > 1 min = cessation of neuronal fxn
permanent damage to brain tissue in 4-5min
51
gingival hyperplasia
phenytoin, nifedipine, verapamil,
52
adverse effects of phenytoin
CNS: cerebeullum & vestibular, ataxia & nystagmus
gingival hyperplasia, coarsening facial features, hirsitism
interfere w/ folic acid absorption
induces P450
teratogen: fetal hydantoin syndrome
53
mechanism of gingival hyperplasia w/ phenytoin
increases expression of PDGF, stimulating prolif of gingival cells & alveolar bone.
54
how are the 3 genes in lac operon coordinated to be made in equal amounts
prokaryotic mRNA can be polycistronic (on mRNA codes for several proteins)
3 genes regulated by SINGLE promoter, operator & regulatory elements
55
duodenal atresia occurs due to..
failure of duodenum to recanalizein early embryonic life
56
malrotation in gut
failure of midgut to rotate counterclockwise as it returns to abdominal cavity
57
when does vitelline duct normally obliterate
7th week
58
aminoglycoside resistance (i.e. via enterococci)
aminoglycoside-modifying agents that transfer diff chemical groups -- acetyl, adenyl, phosphate
outside of bacteria, so it can no longer bind to ribosomes.
aqcuired by plasmid / transposons
59
penicillin resistance
(1) b-lactamase
| (2) penicillin-binding proteins
60
vancomycin resistance
mutation in cell wall precursor turning D-ala-D-ala to D-ala-D-lactate
(altered target)
61
tetracycline resistance
1. mutation in ribosome
| 2. increased efflux, influx
62
fluoroquinolone resistance
mutations in gyrase / topoisomerase gene
63
what is hepatic encephalopathy acutely triggered by
often GI bleed, increasing ammonia & nitrogen in gut for absorption
64
relationship between alpha-ketoglutarate, glutamate, and glutamine
alpha-ketoglutarate + NH3 --> glutamate
(via glutamate dehydrogenase, both ways)
glutamate + NH3 --> glutamine
(via glutamine synthase)
glutamine ---> glutamate + NH3
glutaminase
65
describe glutamate-glutamine cycle
in neuron:
```
glutamate made 2 ways
1. glutamine -> glutamate + NH3
(via glutaminase)
2. alpha-ketoglutarate + NH3 --> glutamate
(via glutamate dehydrogenase)
```
in synaptic cleft, glutamate is taken up by astrocytes
1. glutamate + NH3 --> glutamine
(via glutamine synthase)
glutamine is shuttled back into neurons
66
how does hyperammonia affect glutamate-glutamine cycle
1. in astrocyte, excess NH3 creates toxic accumulation of glutamine
2. in neuron, excess NH3 promotes excess consumption of alpha-ketoglutarate --> glutamate
this leaves less alpha-ketoglutarate for TCA in neurons!
67
which 2 substances are depleted in the brain during hyperammonia? accumulated?
deplete:
1. glutamate
(too much glutamine formation in astrocytes
2. alpha-ketoglutarate
(used to make more glutamate)
accumulate: glutamine in astrocytes! swell
68
oxindole
tryptophan derivative
formed by bacteria in gut & normally cleaved by liver. elevated in hepatic encephalopathy.
69
milrinone
strong ionotropic agent
inhibit phosphodiesterase
increase cardiac cAMP, increased contractility
70
rx: during angioplasty in patients w/ acute coronary syndrome
abciximab
71
deciding between uricosuric (probenicid) agents vs. allopurinol/febuxostat?
if has uric stones, don't want to add more uric acid in urine. give febuxostat / allopurinol.
72
sudden liver failure after surgery?
consider hepatic necrosis caused by halothane!
73
halothane side effects
type 1: aminotransferase elevation, mild syptoms
type 2: fulminant hepatitis. extensive hepatocellular damage.
RAPID ATROPHY - widespread centrilobular hepatocellular necrosis & inflammation of portal tracts & parenchyma
74
decreased albumin levels is a sign of..
chronic liver injury. NOT aute.
half-life of 20 days.
75
presentation of fulminant hepatitis caused by halothane
elevated aminotransferases
prolonged prothrombin
eosinophilia
(albumin takes 20 days to rise)
76
anti-topoisomerase I specific for..
scleroderma (anti Scl-70)
77
characterestics of esophageal motility
fibrosis of distal esophagus
1. esophageal hypomotlity
2. loss of tone in LES
manifests as GERD
78
drug induced lupus
procainamide, hydralazine, isoniazid, d-penicillamine
79
presentation of sjogren
keratoconjunctivitis sicca (dry eye)
xerostomia (dry mouth
may be parotid enlargement
increased risk of non-hodgkin lymphoma
80
anomaly in antiphospholipid syndrome
thombophilia w/ paradoxical increased PTT
81
hydronephrosis vs. autosomal dominant polycystic kidney disease
hydronephrosis: smooth surface
ADPKD: cyst bumps visualized on surface
82
cysts in ADPKD and ARPKD
ADPKD: large cysts, from anywhere.
-lumpy bumpy cysts seen on gross exam of surface
ARPKD: small cysts in collecting duct.
- generally smooth surface
83
shrunken kidney on ultrasound can suggest?
medullary cystic disease -- inherited
tubulointerstitial fibrosis, progressive renal insufficiency. medullary cysts usu NOT visualized.
(shrunken, as opposed to polycystic kidney --> large)
84
mucosa in lactase deficiency
normal
85
pancreatic pseudocyst
potential complication of pancreatitis.
leakage of pancreatic secretions -- induce inflammatory response --> granulation tissue & fibrosis forms to trap fluid
86
cyst vs. pseudocyst
cyst: lined w/ epithelial cells
pseudocyst: granulation tissue
87
most common location for pancreatic pseudocyst:
lesser peritoneal sac, bordered by stomach, duodenum, transverse colon
88
the only radiolucent stone
uric acid stones
89
colorless octahedron crystals
calcium oxalate or calcium phosphate
90
rectangular prism "coffin-lid" crystal
struvite (AMP or triple phosphate
proteus mirabilis / vulgaris, klebsiella, staphlococcus
91
yellow, red-brown, diamond or rhombus
uric acid
92
flat, yellow, hexagonal crystals
cysteine
93
which 2 stones ppt in basic environment
calcium phosphate (or neutral)
AMP
94
inheritance of alpha-1 antitrypsin
co-dominant, affects lung and liver
95
genotype in alpha-1-antitrypsin deficiency
homozygous for Z allele - decrease secretion of A1AT secondary to abnormal protein folding.
STUCK IN ER
96
liver consequences in alpha-1-antitrypsin deficiency
accumulation of anti 1-antitrypsin.
liver issues before lung issues usually
leads to..
1. cirrhosis (2nd most common cause of death) and
2. hepatocellular carcinoma
97
histology of liver w/ alpha 1-antitrypsin deficiency
intracellular granules of unsecreted A1AT.
stain reddish pink w/ PAS
resist digestion by diastase
98
symptoms of scurvy
impaired collagen formation
```
hemorrhage
SUBPERIOSTEAL HEMATOMA
bleeding into JOINT SPACE
GINGIVAL swelling
secondary peridontal infection
anemia
hyperkeratotic papular rash
impaired wound healing
weakened immune response
```
99
vitamin K deficiency vs. vitamin C deficiency
both have bleeding diathesis, but vitamin K usu doesn't present w/ PAINFUL GUMS
100
acrodermatitis enteropathica, growth retardation, infertility
zinc deficiency
101
b-blocker overdose?
glucagon
increase cAMP, increase Ca2+ release during contraction. increases HR & contractility (independent of adrenergic receptors)
102
histological diagnosis of celiac
small intestine: MOST: duodenum and proximal jejuneum
flattening of mucosa w/ loss of villi and chronic inflammatory infiltration of lamina propria
103
antibodies seen in celiac (3)
anti-endomysial
anti-reticulin
anti-transglutaminase
104
common finding in GI malabsorption?
steatorrhea: foul, smelling, bulky, floating, greasy stoof
105
dfiferential of steatorrhea (3)
1. pancreatic insufficiency
- chronic pancreatitis, cystic fibrosis
2. intestinal mucosal defect
- celiac, tropical spru, whipple, chron.
3. bacterial proliferation
small bowel diverticulosis, diabetic neuropathy. bacteria eat nutrients
106
differentiate cause of steatorrhea?
stool sample
1. sudan III stool stain: identidy fat
2. quantitative analysis of amt of fat
then bariums studies to see what caused it.
107
what do you need for diagnosis of malabsorption
STOOL SAMPLE
108
major pathophysiology w/ prolonged NSAID use
chronic interstitial nephritis
clinically: see modest elevation in serum creatinine, evidence of tubular dysfxn, fanconi syndrome (aminoaciduria, glycosuria, hypophosphatemia, hypouricemia)
109
fibromyalgia
key: multiple symmetrically distributed tender spots over patients' muscles, joints, tendons (spine of scapula, lateral epicondyle, medial fat pad of knee)
demo: 20-50y/o. mostly women
widespread musculoskeletal pain w. stiffness, paresthesia, poor sleep, emotional disturbance.
muscle pain & stiffness severe in morning. exacerbated w/ exercise.
110
polymyalgia rheumatica
>50 y/o.
morning stiffness of neck, shoulder, pelvic girdle.
weight loss, fever, increased ESR
111
presentation of ankylosing spondylitis
low back stiffness, resolves w/ exercise.
usu affects males
PE: decrease anterior flexion of spine.
112
formula for clearance
urine concentration x urine flow rate
over
plasma concentration
113
normal filtration rate
~20%
114
common side effects of first-generation anti-histamine
anti-muscarinic
anti-5HT
anti-alpha-adrenergic
and lipophilic --> sedation / cognitive dysfxn
115
second generation antihistamine
NO anti-muscarininc, anti-5HT, anti-alpha-adrenergic.
not lipohilic --> no sedation / cognitive dysfxn
116
hydroxyzine, promethazine, chlorpheniramine, diphenhydramine
1st gen anti-histamine
side effects!
117
fexofenadine
2nd gen anti-histamine
minimal sedation & anti-muscarinic
118
wax & waning lymphadenopathy
follicular lymphoma!
119
follicular lymphoma
most common indolent non-hodgkin lymphoma in adults
indolent course, marked by remission & recurrence
wax & wane
t(14,18) bcl-2 overexpression
120
diffuse large cell lymphoma often involves..
waldeyer ring (oropharyngeal lymphoid tissue)
GI tract
most common aggressive non-hodgkin's lymphoma in adult
121
mycosis fungoides
cutaneous T-cell lymphoma
proliferating CD4+ T cell infiltrate dermis & epidermis --> PAUTRIER MICROABSCESSES.
manifest w/ plaques that may be confused w/ psoriasis or eczema
generalized erythema, scaling, thickening of skin
122
clinical presentation of hairy cell leukemia
splenomegaly & pancytopenia in older men
123
BRAF mutation w/ glutamic acid for valine at position 600 (V600E)
melanoma
124
antibody rx for mutant BRAF in melanoma?
vemurafenib
125
vemurafenib
inhibitor of mutant BRAF in melanoma
126
most common AGGRESSIVE non-hodgkin lymphoma
diffuse large B cell lymphoma
rapidly enlarging mass
127
most common INDOLENT non-hodgkin lymphoma?
follicular lymphoma, wax & wane
