uworld assessment block#1 4.15 Flashcards
definition of ARDS. 1st step & pathogenesis
acute onset lung dysfunction, pulmonary edema, normal left atrial pressure, PaO2/FiO2 noncardiogenic pulmonary edema
CAUSED by injury to ENDOTHELIAL cell lining pulmonary capillaries adjacent to alveoli –> leak fluid into alveoli –> (diffuse alveolar damage) –> hyaline membrane formation –> diffusion barrier, etc.
damage to type II pneumocytes –> fibrosis.
conducitivty of AP in heart.
slowest conduction velocity –> AV node. fastest –> purkinje system.
atrial muscle conductivity faster than ventricular
slowest to fastest:
AV node, ventricles, atria, purkinje
pathognomonic radiograph sign of avascular necrosis
crescent sign: subchondral collapse
radiographic signs of osteosarcoma
destruction of normal trabecular bone pattern, mixed radiodense and radiolucent areas, periosteal new born formation, lifting off cortex, Codman’s triangle. adjacent soft tissue –> ossification –> sunburst
radiographic signs of osteoarthritis
osteophytes and joint space narrowing
4 bony diseases that result from advanced chronic renal failure
(1) hyperparathyroid bone disease (2) osteomalacia (3) mixed uremic osteodystrophy (4) aplastic bone
paget’s disease is associated w/ what other bone problem
osteosarcoma
globus hystericus
globus sensation, or “lump in throat” w/o accompanying physical, endoscopic, or radiologic findings of esophageal obstruction.
common (45% of population)
most – intermittent, some persistent.
often triggered by emotion (fear, tension, anger, mental anguish)
associated w/ organic & functional disorders: GERD, upper esophageal sphincter abnormalities, achalasia, psychiatric disorder, stress
esophageal webs
fragile mucosal folds, cause solid food dysphagia.
pseudobulbar paresis
caused by conditions like MS.
dysarthria, dysphagia, dysphonia, and impaired movt of tongue and fascial muscles
plummer vinison triad
esophageal webs, atrophic glossitis, iron deficiency anemia
zenker diverticulum
false diverticulum. outpouching of pharyngeal mucosa thru acquired defect in muscular wall.
dysphagia, obstruction, halitosis
common sites of endometriosis (decreasing frequency)
ovaries, cul-de-sac, posterior broad ligaments, uterosacral ligaments, uterus, fallopian tubes, sigmoid colon, appendix, round ligaments
adenomyosis
endometrial tissue and stroma within uterine myometrium
pyosalpinx
distension of fallopian tube with purulent discharge
what supplement must be avoided in pregnancy
vitamin A! normally found in leafy vegetables, liver, kidney, egg yolk, butter, accumulates in stellate cells of liver.
excessive vitamin A (usu through supplements) is HIGHLY teratogenic. esp in first trimester. cleft calate, microcephaly, cardiac anomalies, early epiphyseal closure, growth retardation, spontaneous abortion
oseltamivir
sialic acid analogue, inhibits neuroaminidase.
neuroaminodase needed to cleave terminal sialic acid residues on hemaglutinin (so hemagglutinin can attach to cells and respiratory tract mucins)
block prevents release of viron particles
formation of 180 bp fragments of DNA
DNA laddering: sensitive marker of APOPTOSIS. karyorrhexis:
specific endonucleases cleave DNA at internucleosomal linker regions.
helps distinguish from necrotic tissue
dicyclomine, hyoscyamine
antispasmodics
drugs w/ common anticholinergic effects
(1) antihistamines (2) antipsychotics (3) antispasmodics (4) TCAs
methyphenidate, dextroamphetamine, methamphetamine, phentermine
all increase catecholamines at synaptic cleft (block reuptake)
dextroamphetamine also increases release of catecholamines
mosaicism
presents of two or more genetically different cell lines within the body. somatic or germ-line (oocyte / spermatocyte) or both.
usu from a MUTATION in first stages of embryonic development.
when genetic mutation in multiple children but not in parents / family history?
consider germline mutation
important recommendation to diabetic patient
daily foot inspection (infections usu secondary to trauma in setting of preexisting lower extremity vascular and neurologic disease)
fish oil supplementation for…
refractory hypertriglyceridemia
IL-1 is chiefly produced by
mononuclear phagocytes
TNF-alpha is primarily made by..
activated macrophages
IFN-alpha chiefly made by
monocytes, macrophages, B cells and NK cells
what two intercellular linkages depend on cadherins
desmosomes and adherens junctions. desmosomes = intermediate filaments. adherens junction = actin.
cadherins = calcium-dependent.
intracellular: bind to intermediate proteins (catenin, plakoglobin, desmoplakin, which bind to actin/IF)
extracellular: bind toa adjacent cadherin molecule (Ca2+ dependent)
rosacea
first: easy flushing.
later: persistent erythema, telangiectasia, sensitivity to sunlight or insults of chemical/physical nature.
posterior dislocation of tibia most commonly will injury
popliteal artery
(common peroneal and tibial n also at risk, but less susceptible)
common peroneal: lateral knee injury
tibial n: penetrating trauma to popliteal fossa
endometritis caused by
often mixed aerobic and anerobic, but BACTEROIDES commonly isolated.
usu post-partum vaginal or cessarian
nummular eczema
pruitic, coin-shaped erythematous patches.
often occurs in setting of xerosis. exacerbated by use of harsh soaps, environmental toxins.
hormones using RTKs
insulin, EGF, PDGF, VEGF
interviewing techniques: facilitation? reflection?
facilitation: encourage patient to talk more about experience “tell me more”
reflection: repeat what was told. tells patient you listen, allows for clarification.
headache, chronic nasal discharge, atrophic nasal mucosa, thinning of nasal septum, septum perforation, oropharyngeal ulcers, osteolytic sinusitis
long-term intranasal cocaine abusers
allergic rhinitis vs. hay fever vs. vasomotor rhinitis
allergic rhinitis: sneezing, rhinorrhea, nasal congestion, post-nasal drip, pruitis of eyes, nose, palate.
hay fever – seasonal form of allergic rhinitis, provoked by pollen
vasomotor rhinitis – chronic nasal congestion, worsens w/ abrupt changes in temperature or humidity, or exposure w/ odors or alcohol
GFR immediately after nephrectomy? 6 wks later?
immediately after: 50% GFR.
6-wks later: 80%
(hemodynamic & structural adaptations: single nephron GFR rises)
hyperfiltration and hypertrophy of nephron
never 100% again.
sildenafil
promotes erection via relaxation of venous sinus smooth muscle within corpora cavernosa. allows for vascular congestion –> engorgment
amaurosis fugax
symptom of carotid disease, transient monocular blindness
monocular blindness (2)
amaurosis fugax or temporal arteritis
3 places the optic tract terminates
LGN, pretectal nucleus, superior colliculus
damage to long thoracic n caused by? prevents?
caused by axillary lymph node dissection.
C5-7, serratus anterior. unable to raise arm over head and protrustion (winging) of medial border of scapula when outstretched arm is pushed forward agiainst resistance
pec minor articulation
anterior surface of 3-5 ribs, attaches to coracoid process of scapula. medial pectoral n.
bicarbonate rich secretions come from which 2 tissues
(1) exocrine pancreas (2) epithelial cells of billary tract
both stimulated by secretin (S cells in duodenal mucosa)
HCO3 and Cl are inverse. K is stable.
salivary secretion composition
Na, Cl reabsorbed.
K and HCO3 secreted.
high flow rate: more like plasma
sweat composition
hypotonic NaCl. very little HCO3-
acute stress disorder vs. PTSD
SAME symptoms. PTSD > 4 wks
acute stress disorder: following a life-threatening traumatic event. re-experiencing, disturbed sleep, poor conventration, irritable, hypervigilance, restless. distress and impairment.
does NOT last more than 4 wks
schizophrenia & schizophreniform diagnosis
2 or more of: delusion, hallucination, disorganized speech/behavior, negative symptoms.
schizophreniform = 1-6 months schizophrenia = >6 months
false positive formula
1-specificity x no. w/o disease
1- (of people w/o disease, number that test negative)
number need to treat
1/ARR (absolute risk reduction)
acanthomeba infection
immunosuppressed. fatal. accumulates into space-occupying lesions
enzyme deficiency in acute intermittent porphyria (several names for it!)
- porphobillinogen deaminase
- hydroxymethylbilane synthase (HMB synthase)
- uroporphyrinogen I synthetase
congenital erythropoietic porphyria
URO III synthase deficiency (cannot convert HMB to URO III).
severely mutilating: photosensitivity in infancy, erythrodontia, hemolytic anemia
porphyria cutanea tarda
uro decarboxylase deficiency. most common form.
cannot convert URO III –> copro III
tea-coloured urine; blistering cutaneous photosensitivity
hereditary coprophoryria
deficient copro oxidase III. systemic symptoms of AIP with skin findings of PCT
variegate porphyria
deficiency protophry oxidase. HCT with more cutaneous symptoms
erythropoetic protophryia
cutaneous photosensitivity in childhood
pedigree anticipation, difficulty swallowing w/ tongue fasiculations
X-linked bulbospinal muscular atrophy (kennedy disease)
genetic heterogeneity
mutations of different genes cause similar phenotype
reading graphs
read X axis, look at corresponding Y value!!!
osmotic fragility of sickle cells
decreased!
hereditary spherocytosis can cause..
splenomegaly, jaundice, billirubin gallstones (bc of extravascular hemolysis in spleen, increased bilirubin)
splenectomy: improves anemia, decreases hemolysis and jaundice, and reduced incidence of bilirubin gallstones.
3rd heart sound
rapid ventricular filling in mid diastole. sudden deceleration of blood as the elastic limits of ventricular chamber are reached.
normal in children, adults –> ventricular failure.
4th heart sound
forceful contraction of atria pushing blood into overfilled / stiffened ventricle
