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179 Cards in this Set
- Front
- Back
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Diarrhea
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loose &/ watery stool ≥ 3/day
OR an ↑ in volume &/fluidity ± ↑ freq |
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Non-inflammatory Diarrhea
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watery, nonbloody diarrhea
no tissue invasion = no fecal leukocytes |
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Inflammatory Diarrhea
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Colonic Tissue Damage caused by invasion or cytotoxin
blood usually present ± fecal leukocytes absent fever = E Coli O157 H7 |
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Dysentery
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Diarrhea w/ blood & fecal leukocytes
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Tenesmus
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sensation of incomplete rectal evaculation & painful urgency to evaculate stool
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Traveller's DIarrhea
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≥3 uniform stools w/in 24h + other Sx illness w/in 10 days of travelling to another countery
Travel: most common is E coli. Giardia = W & NE US, St. Petersburg & Napal, ≤3wk incubat'n |
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Acute Diarrhea Etiology
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Viral >> Bacterial> Parasites
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Diarrhea Hx:
Copious water Onset 4h postrprandial, 8h, the next day Travel Hx 2 day duration v 25 day duration diurnal vs nocturnal |
Freq: copious watery ≈ small bowel secretion ≈ enterotoxin or viral infx
Onset Two or more persons similarly ill after shared meal: food poisoning <6h of eating: preformed toxin: Staph, Bacillus 6-12h: C perfringes >24h: Bacterial Invasion or ETEC (intraGI toxin formation.) Meds: any new meds before onset suspect; also antibiotics Travel: most common is E coli. Giardia = W & NE US, St. Petersburg & Napal, ≤3wk incubat'n Duration 1-3 days: viral >3 weeks: chronic causes: —Daytime only ≈ "stress related diarrhea" —Nocturnal ≈ Diabetic Neuropathy DM, Hyperthyroidism, Hx rad exposure to abd |
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Diarrhea
AS&Sx: Fever/Chills, Weight Loss, , Alternation w/ constipation, Postural Dizziness, Blood & Mucus, Foul Smelling & Floating |
Fever & Chills: Invasive or Cytotoxic
Weight Loss: CA, hyperthyroidism, malabsorption Alternates w/ Constipation: IBS, obstructing lesion (eg CA) Postural Dizziness ≈ Dehydration Blood/Mucus in stools: Bacteiral infx, IBD, Ischemia, CA Foul smelling & floating stools: malabsorption → spure & parasites |
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Diarrhea
PE focus |
Vitals: ↑T, HR rule in bacterial invasion
Gen: look for dehydration and AMS Abd: look for localized pain & peritoneal signs; true localized tenderness effectively rules out viral & toxin-induced, strongly suggestive of true appendicitis Rectal: fecal impaction ≈ overflow diarrhea; rectal fistulas ≈ Crohns Arthritis, iritis, uveitis, erythema nodosum ≈ IBD Goiter tremor, tachycardia: hyperthyroidism |
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WBC's in stool
Sensitive Test, Rule In, Rule Out |
Microscopic examination has 70% sensitivity
Lactoferrin has 90% sensitivity Invasive organisms: Vast Majority = Top 3: Salmonella, Campylobacter Shigella, (C diff,Vibrio parahemolyticus, Yersinia, Entamoeba histolytica) IBD: UC & Crohns, Radiation Colitis, Ischemic Colitis Rules out: Viral, Vibrio cholera, ETEC, Staph, Bacillus, C perf, Giardia lamblia |
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good table for comparing two main forms of diarrhea
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page 4 acute diarrhea
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Top 3 causes of inflammatory diarrhea due to bacterial tissue invasion
Presentation |
Salmonella: food: eggs, poultry, fruit, vegetables
Shigella: esp daycare children <4yo Campylobacter: chicken, Guillain Barre Cramps Blood/Mucoid Stool Fever Onset is gradual, usu. lasts several days |
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Food Poisoning <12h
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<6:pre-formed toxins:
Staph esp salads w/ mayo Bacillus Ceres rice, starches 6-12: C perf esp meat & gravy allowed to cool all self limited w/in 48h |
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Cytotoxin Induced Inflammatory Diarrhea
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C dif: w/in 2 mo of antibiotics
Vibrio parahemolyticus: shellfish EHEC O157H7: Shiga like toxin; beef, unpasturized juice |
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What is the most important theraputic measu`re in pts with diarrhea & how is it best accomplished
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Rehydration/Preventing Dehydration
oral is preferred method, best is "oral rehydration solution" which contains water, salt, potassium and sugar. glucose and salt transport create osmotic gradient which water follows ORS, commercial or hommade superior to both IV fluids & to CO2 drinks, Juices & gatorade juices, gatorade & CO2 drinks + saltines okay for adults, not okay for peds, too much CHO not enough Na & K 1 tsp salt + 8 tsp sugar + 1L water + 1/2 cup oj or mashed panana for K IV indicated if: shock, AMS, intolrant to roal; NS w/ KCL. |
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Hemolytic Uremic Syndrome
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EHE Coli O157H7
Shiga toxin activates intestinal and renal epithelial cells renal failure, hemolytic anemia, thrombocytopenia esp undercooked hamburger, fresh apple cider w/ cattle feces avoid antibiotics! no fever |
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Discharge instrx for acute non-inflammatory diarrhea
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Rotovirus, Vibrio, ETEC, Staph, Bacillus Ceres, Giardia
avoid colas, milk, ETOH & caffeinated beverages |
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Antipersitaltic Ageqts in Diarrhea
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Loperamide
not considered for children, febrile, or hematocheztic pts. Loperamaide + static EHEC O157H7 toxins → HUS (Thrombocytopenia, Hemolytic Anemia, Renal Failure) |
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Diarrhea Hx:
Apple Cider Stream Water Salads w/ Mayo Undercooked Hamburger Meats Gravies allowed to Cool: C perf Fried Rice Shellfish |
Apple Cider & Undercooked Hamburger: EHEC O157H7
Stream Water: Giardia Salads w/ Mayo Staph aureus Meats, Gravies allowed to Cool Fried Rice, Starches: Bacillus Ceres Shellfish: Vibrio parahemolyticus or if non inflammatory, Norovirus |
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Empiric Rx for Diarrhea
When and What? |
—Given to travellers diarrhea w/ ≥4/day & bloody/pus/mucus stool
—Signs of Bacterial Diarrhea: Fever, bloody, abd pain, fecal leukos —Dehydration or >8/day —Immunocomp —Hospitalization being considered Fluoroquinolone unless suspected EHEC O157H7 (has no fever will cause HUS) antibiotics should not be given to children unless a specific pathogen has been isolated |
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Diarrhea:
Indications for a Stool Cx |
—H&P ≈ invasive diarrhea (Gradual onset, toxic appearance, blood/mucus)
—Fecal leukocyte staining is + for WBC's —Food Handlers —(Immunocomp, IBD) |
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Arthritis, Iritis, Uveitis, Erythema Nodosum
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Crohn's
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Diarrhea
Symptom Management |
Anti-emetics: Prochlorperazine (Compazine) or Promethazine (Phenergan)
Anti-peristaltic: Loperamide (Imodium)not used in febrile, bloody or chidlren Pepto-Bismol: promotes water & Na resporption, inactivates enterotoxins, antibacterial effect, reduces freq of stools & cramping. Immodium works faster, so reserve for febrile, bloody, & children Probiotics reduce risk for and duration of infectious diarrhea [Kaolin-pectin solutions ↓ fluidity of stools but do not Δ dz course] |
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p value
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H0 null hypothesis= the outcome of IV is independent of the input to DV
p is the probability of the null hypothesis being true p<0.05 ≈ very low probability that H0 is true |
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data generated using a device to do the measuring
intervals between numbers are consistently meaningful regardless of location on scale |
Continuous aka Measured Data
normal dist. best represented by mean & standard deviation skewed best represented by median eg BP, height |
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data generated by application of a scale
intervals between numbers arbitrary |
Ranked aka Ordinal data
Medians and Percentiles more appropriate than Means & Variances eg APGAR, Pain Scale |
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data represent counts in each category
no intervals between cateogories |
counted aka nominal, categorical data
cannot calculate means, medians, variances or percentiles mode is only characterization eg: gender, CA grade |
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Box Plot
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Box Runs from 25th percentile to 75th percentile
Whiskers run to extreme value or to 1.5x interquartile range, whichever is shorter outliers (beyond 1.5x IQR) designated by individual dots |
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The Normal Distribution
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average ± 1 standard devation encompasses 68% of pop
average ± 2 standard devations encompasses 95% of pop average ± 3 standard devations encompasses 99.7% of pop |
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Estimating a True Mean
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Point estimation: one number, Δ's w/ every sample
Interval estimation provides confidence interval = Mean ± α* measure of variability most used measure of variability is the standard error of mean SEM = standard deviation divided by the square root of the sample size = σ/√n α = confidence level, standard is 95% ie 95% of all sample confidence intervals will contain the true value of the mean |
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Paired & Unpaired Tests
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In unpaired tests groups of individuals are different (group a received treatment, group b did not)
In paired tests groups are same individuals before and after treatment paired makes each person their own control, takes less difference between groups to achieve significance |
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Tailed Tests
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One Tailed Test
Assume that mean of group 1 > mean of group 2 OR vice versa Two tailed test: assume that the two groups are different without specifying which is larger null hypothesis assumes that mean of group 1 equals number two tailed test would accept null hypothesis out to 2 standard deviations in both directions (95% confidence, 2.5% error on either side) one tailed test (assume that m2<m1) would reject the null hypothesis anywhere beyond 1.6 standard deviations (95% confidence, 5% error on positive side) → smaller differences considered more significant in one-tailed assumptions only justified in using one-tailed assumption if there is already strong evidence which supports that assumption |
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Type I and Type II errors
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Type I: α error, false positive;
conclude that null hypothesis is false when null is true 1 in 20 chance of this with a 95% confidence interval Mn: Agressively Asserting An Arror Type II: β error, false negative conclude that null hypothesis is true when null is false Mn: Backpedal 2 Briskly Usually a 1/5 chance of this, decreased by sample size |
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Means comparison:
two unpaired comparisons two paired comparisons >2 unpaired comparisons >2 paired comparisons |
Parametric and Non-Parametric Means Comparisons
Parametric assumes standard deviation & mean are good descriptors two unpaired comparisons P: paired t test NP: Mann-Whitney U test two paired comparisons P: unpaired t test NP: Wilcoxon signed rank test >2 unpaired comparisons P: Independent measures ANOVA NP: Kruskal-Wallis test >2 paired comparisons P: Repeat measures ANOVA NP: Friedman's test |
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Means comparison:
two paired comparisons two unpaired comparisons >2 paired comparisons >2 unpaired comparisons |
Parametric and Non-Parametric Means Comparisons
Parametric assumes standard deviation & mean are good descriptors two unpaired comparisons P: paired t test NP: Mann-Whitney U test two paired comparisons P: unpaired t test NP: Wilcoxon signed rank test >2 unpaired comparisons P: Independent measures ANOVA NP: Kruskal-Wallis test >2 paired comparisons P: Repeat measures ANOVA NP: Friedman's test |
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Tests of counts
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Non-parametric: Chi squared
No parametric version |
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Tests of correlation
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Parametric: Pearson product-moment correlation
Non-parametric: Spearman rank-order correlation |
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Regression Tests
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Paramatric Test
One IV one DV both normal distribution: Linear Regression Multiple IV's + one normally distributed DV: multiple linear regression Non parametric test: ≥1 IV + Dichotomous DV: logistic regression |
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Nominal vs Normal
Dependent & Independent Variables Which Means Comparison test? |
DV nominal IV nominal = Chi square
DV nominal IV measured: Spearman correlation or logistic regression DV measured & normally distributed: IV nominal 2 levels: T test >2 levels ANOVA Both DV & IV measured & normally distributed: Pearson linear regression |
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T test
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Comparing Two means of normally distributed samples
t = (m1 - m2) /SEM SEM = σ/√n larger the t the more likely the null hypothesis is rejected t can be large because |m1-m2| is large or because SEM is small (small standard deviation/large sample size) |
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Pearson product-moment correlation coefficient
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r
r = 0 no linear correlation (may have non linear correlation) r ≈ +1 strong positive correlation r ≈ -1 strong negative correlation r squared is "coefficient of determination" = fraction of variability in dependent variable accounted for by variation in the independent variable |
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Chi squared
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IV is categorical
DV is categorical chi squared = (observed - expected)squared/expected p value then derived from chi squared value |
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Research Biases
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Selection Bias: subject source bias, Berkson's admission rate bias
—Subject source bias: source in case-control study is hospital records, but hospitals most likely to have severe cases —Berkson's Admission rate bias: looking for assoc. btw two diseases; in case control, people most likely to be in hotpial w/ 2 conditions Information Bias: Recall Bias, Interviewer Bias, Unacceptability Bias. —Recall: people w/ disease ↑ thinking about why they have it, remember risk factors Interviewer Bias: demeanor, thoroughness —Unacceptability: underestimating participation in dangerous behaviors, overestimating healthy behaviors Information Biases side-stepped with biochemical markers > pt interviews Confounding: correlate with true causative variables (poor people live next to airport = poor diet, higher mortality not from airport) |
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Hemorrhagic vs Ischemic Stroke
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Ischemic 4x more common than Ischemic (80/20)
Ischemic caused by local thrombosis or embolism likely to have focal deficits Ischemia of hypoperfusion present w/ bilat neurologic signs Intracerebral hemorrhage into parenchyma Subarachnoid hemorrhage into CSF |
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unilateral lesion
contralateral hemiplegia of face, UE & trunk hemianesthesia homonymous hemianopia gaze pereference to ipsilateral side |
Middle Cerebral Artery
contralateral hemiplegia hemianesthesia homonymous hemianopia gaze pereference to ipsilateral side dominant hemisphere = global aphasia non dominant hemisphere = agnosia & neglect |
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Left Middle Cerebral Artery Stroke
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Hemiplegia of Rt face, UE & trunk
UMN signs in Rt muscles of mastication Rt lower facial expression Rt soft palate failure → Lft Uvular deviation Swallowing Difficulty & Hoarse voice Rt ward deviation of tongue genioglossus Lt sternoclidomasteroid cannot turn head Right Lt trapezius unable to elevate Lt shoulder Rt UE Rt homonymous hemianopia at least or Upper right superior quadrantanopia of Meyer's loop Unable to move eyes to right Executive Fnx impairment Global Aphasia (broca's area, Wernicke's Area & Arcuate Fasiculus) loss of comprehension, fluency and preittion; diffulty writing & reading |
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Right Middle Cerebral Artery Stroke
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Hemiplegia of Left face, UE & trunk
UMN signs in Lt muscles of mastication Lt lower facial expression Lt soft palate failure → Rt Uvular deviation Swallowing Difficulty & Hoarse voice Lt ward deviation of tongue genioglossus Rt sternoclidomasteroid cannot turn head Lt Rt trapezius unable to elevate Rt shoulder Lt UE Lt homonymous hemianopia at least or Upper left superior quadrantanopia of Meyer's loop Unable to move eyes to Left Contralateral neglect loss of spacial awareness contructional apraxia aprosodia (receptive & or expressive) |
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Left Anterior Cerebral Artery Stroke
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Loss of All Sensation from Rt LE
UMN signs in Rt LE Apraxia from loss of supplementary motor area Partial loss of urinary/bowel continence (reflex bladder) Interrupted Papex circuit of cingulate gy → anterograde amnesia Planning & behavioral deficits lack of responsibility, overvalued reward significance, loss of propriety abulia: delay in verbal & motor response |
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Abulia
Paraparesis Urinary Incontinence |
Abulia: delay in verbal &motor reponse
paraparesis: paralysis of LE urinary incontenence from reflex bladder Anterior Cerebral Artery Stroke [From Neuro: Loss of All Sensation from Rt LE UMN signs in Rt LE Apraxia from loss of supplementary motor area Partial loss of urinary/bowel continence (reflex bladder) Interrupted Papex circuit of cingulate gy → anterograde amnesia Planning & behavioral deficits lack of responsibility, overvalued reward significance, loss of propriety abulia: delay in verbal & motor response] |
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Visual Field Deficits as only Neurologic Sign
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Anterior Communicating Artery
most common circle of willis aneurysm |
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Hemianopia with macular sparing
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contralateral hemianopia
Posterior Cerebral Artery Stroke P1 segment: midbrain, subthalamic, thalamic signs P2: corticla temporal & occipital signs |
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PCA Stroke
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contralateral hemianopia
Posterior Cerebral Artery Stroke P1 segment: midbrain, subthalamic, thalamic signs P2: corticla temporal & occipital signs |
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PICA Stroke
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Wallenberg's Syndrome
vertigo, vomiting, nystagmus, numbness of ipsilateral face & contralateral limbs,, ataxia, hoarseness, dysarthrai, dysphasia, and ipsilateral Horner's sro |
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Dizziness, vomiting, jerking eye mvmts, nubness of right face and left extremities, ataxia, hoarsness
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PICA stroke = Wallenberg's Syndrome
vertigo, vomiting, nystagmus, numbness of ipsilateral face & contralateral limbs,, ataxia, hoarseness, dysarthrai, dysphasia, and ipsilateral Horner's sro |
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AICA Stroke
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Isilateral deafness, facial weakness, vertigo, nausea/vomiting, nystagmus, tinnitus, cerebellar ataxia, contralateral loss of pain & temperature sensation
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Pt cannot hear in left ear, is dizzy
facial weakness eyes are jerky left sided loss of pain & temperature sensation |
Right sided AICA
Isilateral deafness, facial weakness, vertigo, nausea/vomiting, nystagmus, tinnitus, cerebellar ataxia, contralateral loss of pain & temperature sensation |
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Posterior Communicating Artery Stroke
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CN3 Nerve Palsey
Down & Out |
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Pt's Right Eye drifts down adn out
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Posterior Communicating Artery Stroke
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Lacunar Strokes
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small penetrating branches
pure motor total hemiparesis = infarct in posterior limb of internal capsule pure sensory stroke = ventrolateral thalamus ataxis hemiparesis = base of pons dysarthria = internal capsule infarction |
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pure motor total hemiparesis
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lacunar stroke with infarct in posterior limb of internal capsule
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pure sensory stroke
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lacunar stroke with infarct in ventrolateral thalamus
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ataxis hemiparesis
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lacunar stroke with infarct in base of pons
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dysarthria
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lacunar stroke with infarct in internal capsule infarction
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Initial Assessment in CVA
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Airway: ↑ intracranial pressure → ↓ respiratory drive; Δconsciousness → intubate
Breathing Circulation The first diagnostic test of a stroke is a Non-Contrast CT of the Brain Stat |
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NIHSS
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National Institutes for Health Stroke Scale
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BP management in strokes
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: ↑ BP likely longstanding (risk of stroke) + phsyiologic response to maintain brain perfusion
Do not treat BP for ischemic stroke unless >220/120 Keep BP of Hemorrhagic Stroke <160/90 Systolic <140 = danger for hypoperfusion ischemia elsewhere |
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CT scan of Stroke
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hemorrhagic: blood in area of stroke: big white blotch
ischemic stroke: CT likely normal, esp <6h |
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Tx Acute CVA
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Admit to ICU
Ischemic Stroke: aspirin is the only effective med; administer full 325 mg dose as soon as CT returns non-hemorrhagic Thrombolytic Therapy for Ischemic is extremely controversial: most effective for salvaging ischemic ts, but pt may convert to hemorrhagic and die the longer ischemia has lasted the more likely TPA → hemorrhage (cut-off 4.5 h now) Hemorrhagic: discontinue all anticoagulants, consider fresh flozen plasma, VitK elevate head to 30*, use analgesia & sedation, osmotic diuretics, NM blockade & hyperventilation to ↓ intracranial pressure Target BP is 160/90 nicardipine drip most common Anti-epileptic tx if seizure start immediate neurosurgical consult |
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2° prevention of CVA
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anti-BP &lipid lowering meds
Tx underlying conditions stop smoking, etoh, Rx |
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Transient Ischemic Attack
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neurologic dysfnx 2° to ischemia w/o acute infarction
10% risk of stroke w/in first 2 days after TIA EKG: tx for a-fib Carotid US: endarterectomy ↓ risk of embolism from carotids Daily Aspirin Therapy Lipid lowering & antihypertensive meds diet& lifestyle mods |
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HA red flags
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Sudden Onset
No Similar Hx Concomitant Infx AMS/Seizure >50 yo Immunosuppressed Visual Disturbances Toxin exposure Neurlogic abnormality ↓ LOC Menigismus ↑/↓ vital signs toxic appearance traumatic findings → urgent non-Contrast CT normal CT → Lumbar Pnx for CSF |
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The Worst Headache of My Life
Thunderclap Onset at 100% Strength |
Subarachnoid Hemorrhage
blood spreads quickly in CSF, rapidly ↑ ICP 50yo ± 10 African American Females aneurysm rupture → vasospastic response → ischemia is the leading cause of death, 50% mortality →non-Contrast CT; normal CT→ Lumbar Pnx for CSF: Xanthochromia (pink/yellow tint) = Hg degradation products MOST SENSITIVE if blood 2° to traumatic entry # of RBC's/tube ↓ as each tube drawn Management: ICU, analgeisa, Serial Transcranial Doppler for vasospasms; stop all blood thinners, seizure prophylaxis; Sugical clipping or endovascular coiling to prevent rebleed. |
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Traumatic Subarachnoid Hemorrhage
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Fairly common concurrence w/ trauma
traumatic SAH not have same complications as spontaneous SAH |
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Bacterial Meningitis
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Inflam'd Leptomeninges, defined by abnormal #WBC in CSF
Classic Triad: Fever, Nuchal Rigidity, Δ Mental Status HA is severe & generalized Brudzinski's sign: flexion of hips in response to passive flexion of neck Kernig's Sign: inability to fully extend knee when hips flexed at 90* Always lumbar puncture unless directly contraindicated CT often got beforehand, but do not delay LP Normal CSF: Protein <50mg/dL, CSF/serum glucose ratio >0.6, <5 WBC/uL; Bacterial: ↑ WBC, Protein, ↓Glucose; Usu. S pneumo or N meningitidis Negative bacterial cultures = viral, most commonly enterovirus <500 WBC/uL, & >50% Lymphos. Protein <100mg, normal glucose; Cannot rule out early bacterial! Viral self-limited; Bacterial much more severe, but looks the same tx both aggressively w/ supportive care, antibiotics and steroids; |
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Involuntary Flexion of Hip with Passive Flexion of Neck
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Brudzinkski's Sign for Meningitis
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Resistance to Knee Extension while Hip is Flexed
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Kernig's Sign for Meningitis
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Migraine HA
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Pt: Females
Path: neuronal dysfnx → intracranial Δ's; not vascular H&P: Phase 1: Premonitory Prodrome in majority: minor signs up to 2 days prior Phase 2: Aura in 25% visual, sensory, verbal or motor; usually brightness or visual loss (scotomoa) Phase 3: HA unilateral, pulsating/throbbing + photophobia or phonophobia ± N/V Phase 4: Postdrome exhuastion afterwards Labs: Unhelpful Abortive Tx: triptans earlier is more effective; Narcotics = rebound HA Preventative Tx: >4/mo, >12h ea or significant disability; antihypertensives, antidepressants, anticonvulsants |
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Tension HA
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Pt: general pop
Path: sensitization of dorsal horn neurons to pericranial myofasical nociception H&P: bilateral constant (non-throbbing) w/o assoc. sx Infreq Episodic <1d/mo Freq Episodic >1d/mo Chronic ≥15d/mo Labs: Unhelpful Tx: Aspirin, Acetaminophen, NSAIDs _ Caffeine Narcotics → abuse & rebounds |
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Cluster HA
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Pt: Males
Path: debated H&P: severe unilateral obital, supraorbital or temporal pain; may switch sides between attacks, but must be unilateral through an attack. ipsilateral ptosis, miosis, lacrimation, rhinorrhea, & nasal congestion Labs: not helpful Tx: O2 |
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Subdural Hematoma
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Tearing of Bridging Veins → Bleed into space btw dura & arachnoid
usu. 2° to trauma 50% mortality Pt: cerebral atrophy: elderly, chronic EtOH, previous traumatic injury fibroblasts will encapsulate the clot w/ collagen over 2 weeks coma in 50% of cases chronic SDH: insidious HA, lightheadedness, cognitive impairment CT: Crescenteric spread around edge TX: ABC's & supportive care Often req's surgical tx to prevent irreversible injury & death from brain herniation Stop taking blood thinners, reverse coagulopatheis |
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Epidural Hematoma
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Pt: young adults 2° to head trauma usu tears middle meningeal Artery
arises in potential space btw dura & skull Sx: highly variable, high suspicion in transient LOC → "lucid interval" → deterioration CT: grapefruit like mass on edge Tx: ABC's supportive, correct coagulopathies majority good recovery mortality ~10% (better in peds than adults) |
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Epilepsy
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recurrent spontaneous seizures from abnormal neuronal firing
Low SE Males Partial seizures = focal localization, may evolve to generalized --simple partial: consciousness not impaired --complex partial: consciousness impaired Generalized seizures = whole of both hemispheres --Absnce seizures: vacant and unresponsive w/ slight twitching --Tonic Clonic: contraction of muscles (tonus) followed by rhythmic muscle contraxns (clonus) Status Epilepticus: continuous seizure activity/successive w/o recovery btw --tonic-clonic >5 min = emergent; consider intubation & induced coma Known Hx Seizures: need more meds, ↑ dose, another med? First Time: full lab workup, CTorMRI + EEG → rule out medical issue (hypoglycemia, hyponatremia) neurlogic illness/injury (stroke meningitis, anoxic ecephalopathy, trauma) Acute: ABC's, fluids prn (BP). IV/rectal Benzos; IV antiepileptics: fosphenytoin, keppra Hospitalization if 1'st w/ prolonged postictal or incomplete recovery Discuss long term prophylaxis w/ neurologist Swimming, Bathing and Driving off limits until seizures controlled |
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Febrile Seizure
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Convulsion ASSx: temperature >38* in a child 6mo-6yrs
No CNS infx/inflam, no metabolic abnormality, no Hx afebrile sz's Common: 1 in 25 children Simple: <15min, no focal features, if in series total <30 min Complex: >15 min, focal feat or postictal paresis or >30 min series Unknown pathology Tx: ABC's, antipyretics; ± glucose, elyte testes; >5min short acting benzos need for anti-epileptic tx rare self limited |
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Common Spinal Cord Injuries
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—Complete: all sensory and motor lost below lvl; acute stage: no UMN signs yet; urinary retention, priapism
—Incomplete: some motor/sensory retained below lvlm sensory more protected than motor, more preserved. —Ventral: anterior spinal artery: weakness & reflex changes from corticospinal tract; bilateral loss of pain and temperature sensation from spinothalamic tract; urinary incontinence —Dorsal: corticospinal tracts, decending autonomic tracts to bladder; gait ataxia, parasthesia, acute LMN signs chronic UMN signs; —Brown-Squard: weakness, loss of vibration and proprioception ipsilaterally and loss of temperature and pain on other side; does not produce bladder sx; —Central: bilateral loss of pain and temperature on several levels, may be normal below, usually cape distribution esp from hyperextension injury in elderly —SCIWORA: Spinal Cord Injury W/O Radiographic Abnormality: Children <8 esp in cervical region; MRI may pick it up. high index of suspicion |
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Traumatic Spinal Cord Injury Management
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Suspect in any trauma victim
Spinal immobilization complete spinal imaging w/ plain film or CT abnormal screening or high suspicion fine cut CT in region urgent surgical consultation to decompress & stabalize ICU in case CV instability/respiratory failure prophylaxis vs DVT-PE Steroids hotly debated, falling out of favor IV methylprednisolone |
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Neurogenic Shock
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Hypotension ± bradycardia 2° interrupted ANS pathways → ↓ vascular resistance
Tx: IV fluids &vasopressors |
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Spinal Shock
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loss of sensation accompanied by motor paralysi w/ initial loss but gradual recover of reflexes
most often occurs after complete cord transection |
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Cauda Equina Sro
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loss of fnx ≥2 of the 18 cauda equina nerves
asymmetric deficits in both legs Bladder involvement if S3-S5 Emergency neurosurgery to decompress nerves and limit damage |
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Eye Kit
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Vision Card
Penlight Fluorescein strips Q tips irrigating Solution Ttetracaine or Proparacain Eye Patch & Eye Shield 1" tape |
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6 Eye Exam Principles
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1. Good Hx
2. Record acuity w/ & w/o glases or w/ pinhole 3. Do not dilate pt w/ possible acute glaucoma or w/ shallow anterior chamber 4. Do notuse atropine 5 Do not use steroids for any positive fluorescein stain of cornea 6. Refer any painless loss of vision pinhole occluder: light only passes into eye from one angle, corrects for distortions at edges of lense or mydriasis |
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Entropion
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Inward Turning of the Eyelid
Tx: surgical referral |
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Ectropion
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Outward turning of the Eyelie
Tx: Surgical Refrral |
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Inflammed Pinguecula or Pterygium
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Tx: artificial tears
topical vasoconstrictors refer if severe |
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Blepharitis
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chronic inflam of lid margin
Types: staph, seborrheic or combo Sx: foreign body sensation, burning mattering Tx: warm compresses, diluted baby shampoo lid scrubs 1-2x daily antibiotic orintment: ciloxin or bacitracin Minocycline 50mg daily Keflex 500mg BID |
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Hordeolum/Chalzion
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Warm Compresses TID
Topical Antibiotics Gram positive coverage Drops for lower lid Ointment for upper lid |
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Herpes Zoster
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Acyclovir 800mg 5x/day
Famvir Topical antibiotics for 2* infx |
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Management of Foreign Body in the Eye
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Topical Anesthetic
On conjunctiva, irrigate or use cotton swab on cornea, irrigate or use sterile hypodermic needle antibiotic ointment p[ressure patch follow up or refer in 24h |
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Corneal Abrasion
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Fluorescein stain
Antibiotic ointment: ciloxin, erythromycin, Bacitracin, Sulfa Pressure patch refer if suspected herpes simplex refer if not healed w/in 48h NO topical anesthetics |
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Hepres Simplex of the Eye
Tx |
Viroptic 5x/day
No Topical Steroids |
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Conjunctivits
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Purulent Discharge = Bacterial
Clear Discharge = Viral Mucosal Discharge = Allergic PReauricular lymphedenopathy signals viral infx |
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Bacterial Conjunctivitis
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Hallmark is Purulent Discharge
Top bacterial causes: staphylococcus, strep, haemophilus tx: topical antibiotid qid 4 days + warm compress; refer if not markedly improved in 4 days |
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Viral Conjunctivitis
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Hallmark is Clear Water Discharge and Palpable Preauricular LN
Commonly accompanies URI, sore throat & fever highly contageous refer if pain, photophobia, or ↓ vision |
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Allergic conjunctivitis
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assoc. w/ hay fever, asthma, ecema
contact allergy: chemicals, cosmetics Tx: topical antihistamines, tears to relieve itching refer refractory cases |
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Prolonged Contact Lens Use, Severe Pain in Early morningq
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Corneal Edema
natural resolution if no corneal abrasion |
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Cellulitis
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Pre-septal: Vision, pupis and motility normal
Tx: oral antibiotics, warm compresses Orbital: pain, fever, blurred vision, diplopia, limited motility, abnormal pupil Tx: eye referral, Hospitalization, blood cultures, orbital CT, ENT consult |
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Tear Deficiency State Sx
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Bruning
Foreign Body Sensation Reflex Tearing Assoc. Conditions: Aging, RA, Stevens-Johnson Sro, Systemic Meds Tx: artificial tears, lubricating ointment hs, punctal occlusion |
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Blow Out Fracture
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Hx Trauma
Check for cision, pupil response, motility, ask about diplopia check cheeek for anesthesia water's vieew orbital x ray, CT positive fx → oral antibiotics &referral |
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Alkali burns
|
reacts with lipids to form a soap, penetrates stroma easily
anhydrous ammonia penetrates rapidly Tx: topical anesthetic, irrigate with few liters of saline, inspect for particles, refer |
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Acid Burn
|
Rapidly neutralized by tears and cells
usually doe snot penetrate stroma Tx: same as alkali burn, topical anesthetic, irrigate with few liters of saline, inspect for particles, refer |
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Diabetic Retinopathy
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4th most common cause of visual loss in elderly
macular edema more common with T2DM minimize effects with good glycoemic control |
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Retinal detachment
|
floaters, flashes of light
"curtain" or "veil" peripherally ± ↓ vision |
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CN palseis of the eye
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± caused by systemic ischemic disease
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temporal arteritis
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vasculitis affecting medium-sized vessels
may cause ischemic optic neuropathy CN palsies retinal vascular occlusions Sx: HA, malaise, night sweats, weight loss, jaw claudication, molymyalgia rheumatica Dx: clinical w/ temporal artery biopsy, giant cell infiltration is specific Px: ± vision loss if unTx Tx: oral corticosteroids, start tx on dx, biopsy not affected if done w/in 1 week of tx |
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ALS
Condition, Pathogenesis, Risk Factors |
aka motor neuron disease, the most common pure motor disease
progressive weakness in single region s pain, ↓ sensatn or incontinence; continuous progression s ↑↑ or ↓, eventually spreads to all regions lose LMN's, UMN's & prefrontal motor neurons (→ dementia) onset peaks 80 yo, uniformly fatal avg 3 years 90% spont: TDP-43 mutation → TAR DNA binding protein cytoplasmic incl., glutamate toxicity 10% familial mutation of SOD-1 gene both oxidative damage: apoptosis, defective axonal transport Risk Factors: smoking, cycad foods |
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facial weakness, poor palatal elevation dysarthria
tongue atrophy and fasiculations all sensation intact |
Bulbar ALS
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motor weakness in neck, shoulders, UE
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Cervical ALS
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motor weakness in chest, abd
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Thoracic ALS
SOB & orthopnea |
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Motor weakness in lower back, groin, LE
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Lumbosacral ALS
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ALS
Complications Electrodiagnostics Tx |
Complications: ≠ ADLs, ambulation; aspiration pneumonia, resp insuffic. decubitus ulcers, DVT-PE
Electrodiagnostics: ↓ amp. of muscle AP's; normal peierphal nerve condxn veloc's, miexed apptern of actue denervation & chronic renervation at multiple lvls Tx: Noninvasive ventilation, PEG, Riluzole (glutamate antagonsit) Supportive care: --communicate Dx & Px --Δdiet for dysphagia --computer aided speech --benzos or MS to relieve dyspnea --N acetylcysteine or amitryptyline vs secretions --spiritual and psychological care; pts fear choking to death. 90% will die peacefully of hypercapnea in sleep |
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Riluzole
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glutamate antagonist used in ALS
extends life by 2-3mo SE: GI, asthenia |
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Multiple Sclerosis
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chronic inflammatory demyelinating CNS dz c periventricular infiltrates of lymphos & monocytes → wide variety of neruologic manifestations
"The Viking Theory" N Euro Ancestry HLA DRB1-1501 ↑ BBB VLA4 adhesion molecules, ↑ IgG in CSF; Th17: Proinflam IL12 & IL17 Onset any age, most commonly working adult life attack vs myelin sheath, wide variety/odd combos of neurologic sx's new attacks periodically with new neurologic sx remyelination occurs, but plaques cause permenent dysfnx often → wheelchair bound; LE ↓ 6yrs, death 2° disability (3* to dz) |
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MS Dx
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Hx
Oligoclonal banding in CSF electrophoresis (indicative of elevated CSF [IgG]) IgG index Rule Out: HIV, SLE, Vasculitis, Lyme Gold Standard: MRI c gadolinium: --Gadonlinium enhances visualization of T2 weighted hyperintense lesions: ovoid and limited to white matter in periventricular area in both brain and spinal cord. Lesions ↑↓ in size and intensity. --T1 holes are T1 weighted hypointensities indicative of non inflammatory neurodgeneration, worse prognosis. |
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MS Tx
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Tx Acute flares c IV glucocorticoids
Support: Depression common suicide 7x general pop Rehab, Social issues, manage complications (2* to focal deficits) early aggressive tx ↓ attack rate & progression; indicated if cranial MRI is abnormal at first presentation or w/in 6 mo of event; long term success not sure beyond 2 years Glatiramer (copaxone) mix of random polymers of 4 AAs: glyamate lysein, alanine and tyrosine) similar to myelin basic protein. compete w/ MBP for MHC presentation to T cells; also induces Th2 anti-inflam activation. Interferons INFB-1b (betaseron) INFB-1a (Avonex) ↓ inflam by inhbiting: INFγ & adhesion molecules, MMP 6 & 9 prodxn, transmigration of inflam cells across BBB; SE: ± neurtalizing abs, flu like sx & injx site rxn common Monoclonal antibodies natalizumab antegren impair integrin adhesion molecule on T lymphos; Immunosuppressives & Statins: Δimmunity |
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Parkinson's
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loss of domaminergic neurons of the substantia nigra, presence of lewy bodies and lewy neurities
onset ~60, rare <40 Cardinal Signs: Resting Tremor, Rigidity, Bradykinesia, Postrual instability Dx: histopathology Probable: 3/4, responsive to levodopa or >3yrs Possible: 2/4 <3 yrs or no levodopa trial Nonmotor: depression, Δsleep, pain (psychosis, fatigue Δolfactn) Complixn's: Dysphagia c aspiration, ANS dysnfx → orthostasis, 1/3 have dementia onset 8 years Px: highly variable; poor Px: older, male severe sx, ↓ responsive to tx, w/ dementia & comorbidities Tx: levodopa, dopamin antagonists (pramipexole &^ ropinorole) anticholinergics (trihexyphenidyl), amantadine; usually good control for ~5 yrs; SE common |
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Age of Neurodegenerative Pts
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Parkinsons: onset ~60, rare <40
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Essential Tremor
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Most common cause of tremor 5% of pop
usu. symmetric intention tremor or isolated head tremor w/ Family Hx otherwise neurologically normal |
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most common cause of tremor
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Essential Tremor 5% of pop
usu. symmetric intention tremor or isolated head tremor w/ Family Hx otherwise neurologically normal |
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Top Causes of Peripheral Neuropathy
|
1. Diabetes
2. EtOHism 3. CT disease |
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diabetic neuropathy
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50% of diabetics will eventually dvlp neuropathy 2* to small vessel ischemia & hyperglycemia
Frequently present at onset of T2DM initially intermittent pain and tingling in feet, later pain becomes more intense and constant. Eventually painless neuropathy with loss of sensation. Almost no loss of motor function. Most commonly: Stocking/Glove Distribution Diabetic Thoracic Radiculopathy: Burning, stabbing belt like pain, usually unilateral along >= spinal roots. Mononeuritis: painful sensory & motor neuropathy of one peripheral nerve (eg Peroneal N) Mononeuritis multiplex: painfule sensory & motor neuropathy of at least 2 separate nerve areas, more likely to be systemic disease (DM, vasculitis, amyloidosis) |
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Describe the pathogenesis of hyperglycemic effect on nerve function.
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Advanced Glycation End Products: intracellular glucose derived dicarbonyl precurosors + amnio groups of proteins; resistant to protesolytic degredation, rate of prodxn increases in hyperglycemia
AGE can directly crosslink polypeptides, decreases large vessel elasticity, & makess it sticky, trapping LDL's → atherogenesis Receptors = RAGE; Rage + AGE → -M0 release cytokines, growth & procoagulant factors -endothelial cells produce ROS's & procoagulant activity -VSMC proliferate & synth ECM AGE in capillaries & glomeruli traps albumin in basement membrane = diabetic microangiopathy Polyol Disturbances Tissues which do not req insulin for glucose transport: especially nerves and lenses NADPH used in reaction aldose reductase glucose → sorbitol; NADPH not available to regenerate GSH → ROS damage; glucose neurotoxicity. |
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Exanthem v Enanthem
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Exanthem = skin rash associated with a viral infection
Enanthem = rash on the mucosal surfaces associated with a viral infection |
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High fever for 3-4 days followed by defervescence with the appearance of a subtle erythematous macular rash at that time that lasts for 24 hours. Usually there are no physical findings to explain the fever and the child looks well. The rash is most typical on the trunk and neck. 80% of cases occur before 18 mos.
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Exanthem subitum (roseola infantum):
The incubation period is an average of 12 days. Roseola is a major cause of febrile seizures and ER visits. Causative agent-Human Herpes Virus types 6 & 7 Treatment-symptomatic only, ie. treat the fever. |
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Begins with symptoms of a mild URI and mild fever. There is significant tender retroauricular, posterior cervical, and posterior occipital lymphadenopathy. In some, an enanthem covering the soft palate may appear prior to the onset of the rash. The exanthem usually begins on the face and spreads to cover the trunk. It is maculopapular, with areas of confluence and flushing. Mild pruritis is common and the rash clears by the 3rd day.
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Rubella (German Measles):
In general, the rash of rubella is not as prominent as the rash of Rubeola, and the patient has a less severe disease picture, with a lower degree of fever. Causative agent-An RNA virus in the family Togaviridae, genus Rubivirus Treatment-symptomatic only |
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Prodromal phase has a low-grade fever and the “3 C’s” (cough, coryza, conjunctivitis), which are followed by grayish-white spots with slight reddish areolae opposite the lower molars in 2-3 days. Photophobia is common. The temperature rises abruptly as the skin rash appears. The rash usually begins on the face and neck and spreads over the entire body from the neck down.
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Rubeola (red measles):
Mnemonic-cc-CPK (c=cough; c=coryza; C=conjunctivitis; P=photophobia; K=Koplik’s spots) Causative agent-Parmyxovirus Treatment-symptomatic only |
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Presents with fever, chills, headache, vomiting, and pharyngitis. The tonsils are hyperemic, edematous and may be covered with an exudate. The rash is papular and has the texture of coarse sandpaper. It begins in the axillae, the groin and the neck and within 24 hours becomes generalized. Desquamation begins on the face and proceeds to the hands and feet and may last for 6 weeks.
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Scarlet Fever:
Causative agent-group A beta-hemolytic streptococcus Treatment-Penicillin V |
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Begins as a low-grade fever and produces a “slapped cheek” appearance on the face associated with a lacy, reticular-like macular rash on the trunk and extremities. The slapped cheeks appear first, then the rash on the extremities comes about 2 days later. Constitutional symptoms may include headache, pharyngitis, myalgias, arthritis and malaise. A
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Erythema infectiosum (fifth disease):
dult women develop an arthritis similar to RA that may persist for 4 years. More than ½ of adults have serologic evidence of prior infection. In pregnant females, the fetus may become infected causing edema (fetal hydrops). Causative agent-parvovirus B19 Treatment-symptomatic only |
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Fungal Infections
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Tinea pedis (Athlete’s foot)—Most commonly maceration between toes, but can also present in a moccasin fashion with dry scaling on the sole of the foot.
Tinea Cruis (“Jock itch”) Tinea Capitus (scalp)-scaling, alopecia, and broken hairs at the scalp. Must use oral antifungals to treat. Tinea corporis (“ringworm”) Causative agents for the above 3 tinea infections: Dermatophytes (fungi that have the ability to live on the keratin, ie. Hair, nails, and skin) (Microsporum, Trichophyton & Epidermophyton) Diagnosis is KOH prep showing hyphae Treatment for the above 3 tinea infections other than tinea capitus—Topical antifungals such as clotrimazole, ketoconazole, terbinafine, ciclopirox |
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asymptomatic oval macules on the chest and back either hypopigmented, pink, or brown with a very fine scale
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Tinea Versicolor (pityriasis versicolor):
Causative agent—Malassezia globosa (Please note that older references will state that it is Malassezia furfur, but newer studies show it is globosa) Treatment—Nizoral (ketoconazole) shampoo or cream or selenium sulfide Shampoo. |
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erythematous plaque with satellite lesions in warm moist areas of skin
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Candidiasis
Causative agent—Candida albicans Treatment—Topical antifungals such as clotrimazole, ketoconazole, or nystatin |
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Sharply demarcated, scaly, coin-shaped lesions that mimic ringworm. Most common in dry winter climates and in atopic individuals
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Nummular (Discoid) Eczema:The cause is unknown.. The lesions last months to years and are some of the most treatment-resistant forms of eczema. The treatment is topical steroids, plastic wrap and emollients.
Contact Dermatitis: |
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Irritant Dermatitis
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80% of contact dermatitis is irritant dermatitis. Given enough irritant exposure, anyone’s skin can develop an irritant dermatitis.
the acute toxic blister eruption that can occur from a single exposure to a strong chemical and a chronic repetitive exposure to lesser irritants. In an acute toxic exposure to something like an acid, symptoms typically occur a few minutes to several hours after exposure. This is not an immunologic response. It can occur on the first contact with the substance as no previous exposure is necessary. Chronic irritant contact dermatitis can occur from excessive use of bleach, rubbing alcohol or detergents, and may take weeks or months to develop. The hands are the most common site and the skin will be erythematous, chapped and dry. There will usually not be vesicles in this type. Treatment—Decreasing exposure to the substances and increasing the use of emollients with occlusion; protective gloves or clothing. |
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Latex Dermatitis
|
type IV hypersensitivity allergic contact dermatitis or an irritant dermatitis
main concern is a type I, IgE-mediated anaphylaxis. True latex allergy causes hives on the hands shortly after putting on the gloves. |
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Allergic Dermatitis
|
The rash usually occurs 1-2 days or even a week after exposure. The cause does not have to be a new substance. An allergy can develop at any time, to any product, even after years of contact. Exposure to a strong sensitizer such as poison ivy results in sensitization within a few days, whereas exposure to a weak allergen may take months to years for sensitization. Common allergens are poison ivy/oak/sumac, nickel, neomycin (13% of the population is now allergic), bacitracin, rubber, fragrances, adhesive tape.
Exam findings range from erythema and papules to vesicles with weeping and crusting. Poison Ivy classically has linear lesions representing contact with the stems of the plant. |
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Atopic Dermatitis
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“The itch that rashes”. ALL of these patients itch! The distribution is commonly on the cheeks in infants and the antecubital and popliteal areas in children. Patients tend to either have a history of dry skin, asthma and/or hayfever, OR, they later develop allergic rhinitis (70%) or asthma (50%). Because the patients tend to have these other allergic issues, they may have an eosinophilia or elevated IgE. They may complain of being “sensitive” to scented creams or dryer sheets. It usually occurs in infants and children, with 90% presenting in the 1st year of life.
Patients with atopic dermatitis will often also have keratosis pilaris. |
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A chronic condition of occlusion and secondary infection of the hair follicles. Pustules, nodules, abscesses and scarring can occur.
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Hidradenitis suppurativa
Treatment—antibacterial soaps, systemic antibiotics, intralesional steroids, surgery |
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Erythema, telangectasias, papules, and pustules of central face. NO comedones as seen in acne vulgaris. It is exacerbated by heat, alcohol and spicy foods.
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Rosacea
Treatment: Avoidance of triggers and topical metronidazole gel. |
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Erythematous, edematous plaques (wheals).
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Urticaria (hives): There are multiple causes (food, drugs, infections, etc) but idiopathic is the #1 cause. The treatment is avoidance of known triggers and antihistamines.
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tender pink to dusky red firm nodules on the extensor surfaces of the extremities that fade like a bruise over a month. These nodules may appear semi-flat on the surface, but when palpating you will note that they extend down into the SubQ and are nodular in nature
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Erythema Nodosum
TB (may see EN before PPD is + because that takes 6-8 weeks) (TB assoc. EN is much less common these days) Cocci beta-hemolytic strep (Can be seen even weeks after the infection) sulfonamides (Can be seen even weeks after treatment) oral contraceptives sarcoidosis ulcerative colitis pregnancy Hepatitis B Chlamydial infections idiopathic in 40%. |
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A systemic disease characterized by violaceous (heliotrope) inflammatory changes of the eyelids and periorbital area, erythema of the face, neck, and upper trunk, and by flat-topped violaceous papules over the knuckles (Gottron’s papules). All have bilateral proximal muscle weakness and elevated muscle enzymes (CPK).
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Dermatomyositis
This is associated with underlying malignancies, especially ovarian, breast, lung, stomach, colon and uterus. |
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There are rough, small, hyperkeratotic papules at the orifice of hair follicles on the extensor surfaces of arms and thighs.
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Keratosis Pilaris:
An autosomal dominant trait. . They are basically due to plugging of the hair follicle. It is very common in children and adolescents, especially if they are atopic. It affects 50-80% of all adolescents to some degree and 40% of all adults. If it persists to adulthood, it usually persists indefinitely. It is asymptomatic, but is a cosmetic concern for some. The skin will feel like sandpaper. Abrasive washes, tight clothes and scratching aggravate the condition. LacHydrin cream has keratolytic properties and will gently exfoliate the area and decrease the roughness as well as hydrate the skin. |
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Epidermal hyperkeratosis with a fish scale appearance.
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Ichthyosis:
Ichthyosis Vulgaris- is autosomal dominant and these patients will have dry skin, rectangular scaling and keratosis pilaris. It begins to appear in childhood. It is fairly common with an incidence of 1 in 250 to 300. X-linked Ichthyosis-This is not nearly as common (1:6000). Will only affect males and presents shortly after birth. Caused by a deficiency of steroid sulfatase. Treatment-aggressive moisturization with emollients such as Aquaphor and use of keratolytic agents such as Lac-Hydrin (lactic acid) or Aqua glycolic (glycolic acid). These patients will have to be treated for life. |
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An asymptomatic, usually singular, skin tumor, sometimes associated with a history of trauma. They are common on the legs of adults. There is usually a + dimple sign
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Dermatofibroma: benign skin tumor
tx: reassurance |
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An asymptomatic overgrowth of epidermal cells within a cyst wall. There is usually an overlying pore and if you squeeze, you may express a foul-smelling cheesy material.
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Epidermoid cyst
They are removed for cosmetic puposes. |
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A tumor of the subcutaneous fat, not really the skin
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Lipoma benign
Reassure the patient unless it is large enough that it is causing pain. |
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Pigmented, waxy papules and plaques with a warty surface and “stuck-on” appearance.
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Seborrhea Keratosis. Reassure patient and remove those lesions patient asks to have removed for cosmetic purposes.
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ABCD’s of Premalignant and malignant skin tumors
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Asymmetry
Border (irregular) Color (variegated) Diameter (>eraser) |
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Slightly erythematous, scaly papules on sun-exposed areas. They feel rough.
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Actinic Keratosis
Treatment is cryotherapy. |
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A herald patch, which is a solitary, round lesion that may occur anywhere on the body, precedes the generalized maculopapular eruption of oval or round lesions. The long axis of the oval lesions follow the lines of skin stress in a Christmas tree pattern.
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Pityriasis rosea:
Causative agent-unknown Treatment-symptomatic only |
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A localized plaque or multiple areas of chronic inflammation caused by habitual rubbing and scratching. Only excoriated lesions are seen. The center of the back is typically spared.
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Lichen Simplex Chronicus:Treatment includes a complete stopping of the scratching by the patient as well as antihistamines, topical steroids and stress reduction
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Granuloma Annulare
|
-Self-limited, chronic inflammation of unknown origin. It is asymptomatic, occurs mainly in children and young adults and resolves spontaneously within 2 years. It begins with a flesh or reddish-purple papule that then undergoes central involution and develops into a ring-like lesion.
Differential diagnosis includes cutaneous larvae migrans and tinea. With tinea, you would expect to see scaling at the border. |
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on the soles of the feet in patients who have been walking in moist feces-contaminated sand on the beaches of the Caribbean, South America and Africa.
itching and an elevated eosinophil count |
Cutaneous larvae migrans (CLM) is caused by the hookworm larvae underneath the skin.
Untreated, the larvae die in 2-8 weeks and are eventually sloughed off. Albendazole can be used x 7 days po to treat. |
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Fluid Replacement in Heat Illness
|
Cool Liquids by Mouth preferred in alert pts
Room Temp Isotonic Crystaline liquids IV for unconscious |
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Heat Cramps
|
Dilutional hyponatremia from water only fluid replacement
cramping of muscles being used not uncommon in conditioned athletes DDx: Anxiety, Diuretic Use → hyperventilation, hypocalcemia, hypokalemia Tx: oral fluid/elyte replacement |
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Risk Factors Heat Stroke
|
Heat Load: temp, humidty, Env (e.g., full sun exposure), Work or exercise
Illness: CV compromise/disease, Dehydration/hypovolemia, Spinal cord injury associated with impaired sweating, Impaired mentation, Skin or sweat follicle abnormality, Burns, CF, Ectodermal dysplasia (congenital absence of sweat glands), Scleroderma, Parkinsonism, Pheochromocytoma, Hyperthyroidism, Obesity Anticholinergics, antihistamines, phenothiaszines, cyclic antidepressants: inhibit sweating Amphetamines, phencyclidine, LSD, cocaine: ↑ metabolic activity Diuretics, Alcohol Previous history of heat stroke, Lack of acclimatization, Fatigue, Lack of sleep, Infection, Constrictive clothing, Extremes of age |
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|
Diagnostic Workup for Heat Stroke
|
CBC: WBC >30k or w/ bands ≈ underlying infx
dilutional ↑ Hg & HCT ; ↓ ≈ anemia, occult bleeding elytes: ↓Na, P, K; ↑K ≈muscle breakdown UA: hydration status, rhabdo ( + hg c - RBCs) Liver Enzymes: Liver damage a common complication Serum Glucose: ± ↑/↓ ABG: PaO2; Lactic acisosis ≈ severe Coagulation profile for DIC Cx: Blood & Urine: sepsis more common than heatstroke CXR: pneumonia CT: Subarachnoid hemorrhage EKG: MI, dysrhythmias 2° CV stress |
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Complications of Heat Stroke
|
Shivering: tx w/ chlorpromazine IV
Hypotension: fluid replacement w/ central venous monitoring to prevent overload esp pulmonary capillary wedge pressure; dobutamine Rhabdo: mannitol for osmoticc diuresis to UA of 70 mL/h; alkalinze urine via NaHCO3 to prevent precipitation Renal failure: usually reversible req's temp dialysis |
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Heat Exhaustion
|
Occurs gradually over a period of days
water only replacement → dilutional hypnoatremia no water → dehydration hypernatremia more risk heat stroke No mental status changes (possible heat syncope) low morbidity &mortality, but on continuum w/ heat stroke Tx: oral rehydration, observe 6h, release no exercise/heat exposure for 72 h. admit w/ ongoing sx like vomiting orthostatic hypotension or potential complciation |
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Heat Stroke
|
body's heat loss mechnisms overwhelmed
older persons over days; may even stop sweating younger people exertional heatloss, probably stilll sweating high fever w/ neurologic deterioration: presents as AMS, focal deficits, seizure or coma 20% mortality complixns: hepatic failure, DIC, Rhabdo & Renal failure in exertional Tx: admit to ICU agressive monitoring |
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Heat Syncope
|
Volume Depletion + Peripheral Vasodilation → postural hypotension
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Ottowa Rules
|
Ankles Series Req'd if any pain in Maleolar zone and
Bone tenderness at posterior edge or tip of lateral malleuolus Or boone tenderness at posterior edge or tip of medial malleolus OR Inability to bear weight both immediatley and in the ED A foot series is required if there is any bone tenderness at the base of the metatarsal, at the navicular or inability to bear weight both immediatly and in the ED |
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|
Description of Fracture
|
Which bone
which part salter as applicatble configuration and type displacement shortening angulation rotation |
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|
Salter Classes
|
1: S separation at palte
2: A through plate into metaphysis, most common (Above) 3: L through plate into epiphysis (Lower) 4: T through metaphysis and epiphysis (not along plage) 5: ER: Erasure of physis (compression) least common |
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Elbow Ossification
|
Come Rub My Tree Of Life
Capitulum 2 yo Radial Head 4 yo Medial epicondyle 6 yo Trochela 8 yo Olecranon 10 yo Lateral epicondyle 12 yo |
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Elbow Fat Bat Visible
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Sail Sign
|
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Boney Rings
|
Pelvis, Mandible, Forearm, Lower Leg, Stapes
With any boney ring fracture, always search for a 2nd fracture or dislocation |
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|
Montaggia Fx
|
mid-shaft ulna fracture assoc w/ radial head dislocation
(With any boney ring fracture, always search for a 2nd fracture or dislocation) |
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|
Triage of Fx
|
Immediate Orthopedic Referral:
Obvious deformity Significant Physial Injury 3-5 or displaced 1&2 open/complex (spiral, comminuted, compression) Intraarticular fx or penetrating wounds NAV compromise Any Femur, spinal, pelvic fx's Complete or displaced LE fx ED management with Ortho fu Nondisplaced slater 1 (except femur & proximal tibia) Clavicular fx Incomplete UE fx, LE long bone w/ mild deformity Uncomplicated hand or foot Routine dislocation of shoulder or minor joints w/o fx |
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Splint care
|
Rest & elevate 24-48h
analgesics for pain if fingers toes swollen, cold pale etc, rewrap bandage, if not releived, return to ED keep dry do not stick ojbejcts under splint to relieve itching fu w/ orthopod w/in 7 days |
