OK I know this sounds stupid but I have a friend that gets really freaked out before big tests like finals, HESI, NCLEX, and usually we get together and a few days before I start throwing out random facts at her. On 2 different tests she said the only way she got several questions was from the random facts that I threw at her that she never would have thought of!
SOOOOO..... I thought that if yall wanted to do this we could get a thread going and try to throw out 5 random facts or "things to remember". NCLEX is coming and the more I try to review content the more I realize that I have forgotten so......here are my 5 random facts for ya:
OH and BTW these came from rationales in Kaplan or Saunders no made up stuff:
1️⃣ A kid with Hepatitis A can return to school 1 week within the onset of jaundice.
2️⃣ After a patient has dialysis they may have a slight fever...this is normal due to the fact that the dialysis solution is warmed by the machine.
3️⃣ Hyperkalemia presents on an EKG as tall peaked T-waves
4️⃣ The antidote for Mag Sulfate toxicity is ---Calcium Gluconate
5️⃣ Impetigo is a CONTAGEOUS skin disorder and the person needs to wash ALL linens and dishes seperate from the family. They also need to wash their hands frequently and avoid contact.
Oh, ohh, one more...
? Vasopressin is also known as antidiuretic hormone
[color=#2f4f4f]prescribed for manic episodes/bipolar disorder
[color=#2f4f4f]symptoms of toxicity begin to appear when therapeutic level is 1.5 - 2.0
[color=#2f4f4f]serum level 1.5 (mild toxicity) symptoms include mild ataxia, some muscle weakness
[color=#2f4f4f]serum level 1.5 - 2.5 (moderate toxicity) symptoms include n/v, severe diarrhea, slurred speech, blurred vision, muscle twitching
[color=#2f4f4f]serum level > 2.5 (severe toxicity) symptoms include nystagmus, deep tendon hyperreflexia, impaired loc, tonic-clonic seizures or coma, leading to death
[color=#2f4f4f]digoxin 0.5 - 2
[color=#2f4f4f]loading dose is usually 0.5 1.0 mg iv/po in divided doses over 24hrs
[color=#2f4f4f]maintenance dose is usually 0.125 - 0.5 mg iv/po
[color=#2f4f4f]prescribed for heart failure and cardiogenic shock
[color=#2f4f4f]monitor potassium level--if potassium drops pts become dig toxic quickly
[color=#2f4f4f]serum level > 2.0 (toxic) symptoms of dig toxicity include n/v, visual disturbances (greenish-yellow halo), confusion
Today I will have my examinations. You know how important they are to me. So I am humbly asking Your gracious help and divine assitance. I pray to you, my dear God, please neve rlet me be at ease and give my very best. Please never let me guess nor rely on pure luck, but enlighten my mind and let me think clearly. Please never let me resort to chances nor to dishonesty, but let me work to the fullest of my ability. I pray for Your guidance that i as i think, I may find the right solutions, I may be able to correctly answer the questions, I may solve those difficult problems. I ask, O God, Your intercession, that as I write, I may not be careless nor overconfident, I may not be distracted but be more concentrated, I may not be in a hurry nor take the exams too lightly. Today, O my Lord, I will take my examinations Let me, with Your help, give my best effort. Let me, because of You, receive the best and fruitful results. This I pray in Jesus name. Amen.
it is useful to divide this class into the usual medical pathologies caused by each
•urinary pathogens
[color=#009900]–e. coli
•normal intestinal flora cause [color=#ff6666]90% of uti; also [color=#ff6666]pyelonephritis
•pathogenic varieties are not normal flora and can cause infectious diarrhea, hemolytic anemia
•tx: [color=#3333ff]ciprofloxacin or bactrim (zosyn also effective)
[color=#009900]–proteus
•causes [color=#ff6666]uti, in addition to [color=#ff6666]renal calculi (struvite, caco3)
•tx: [color=#3366ff]levaquin or bactrim (often treated without knowing you are treating proteus)
•respiratory pathogens
–[color=#009900]haemophilus influenzae•cause: [color=#ff6666]pneumonia, aom; also sepsis, meningitis, cellulitis
•tx: [color=#3366ff]azithromycin
–also susceptible to po 3/4 gen cephs, augmentin, doxycycline, quinolones, carbapenems
–[color=#009900]klebsiella pneumoniae•usually only pathogenic in hospitalized immunocompromised causing [color=#ff6666]pneumonia and/or sepsis
•rapid resitance develops, especially against cephalosporins and quinolones
•s/s: [color=#ff6666]profuse, jelly-like, bloody sputum and high mortality rate
•tx: [color=#3366ff]carbapenems or zosyn
[color=#009900]–legionella
•[color=#ff6666]pneumonia, derived airborn from water ducts, air conditioning units, water towers
•tx: [color=#3366ff]macrolide (or quinolone or doxycycline)
–[color=#009900]pseudomonas aeruginosa
•opportunistic infection causes [color=#ff6666]pneumonia, sepsis, uti, right side endocarditis, osteomyelitis in diabetic foot ulcers
•first s/s often overwhelming [color=#ff6666]gram negative sepsis; 2nd most common cause of infection in icu
•extremely resistant to many drugs; all effective drugs iv, except cipro and levaquin so their use is severely restricted to avoid development of resistant strains
•tx: [color=#3366ff]ceftazidime and gentamycin (or imipenem or zosyn- varies widely between hospitals)
–also susceptible to the following: tobramycin, cefipime, colistin, aztreonam
–[color=#009900]acinetobacter•[color=#ff6666]pneumonia, sepsis, shock common, up to 70% mortality; can live 3 weeks on dry surface
•tx: [color=#3366ff]imipenem
–colistin or doxycycline is alternative
•gastrointestinal pathogens
–[color=#009900]helicobacter pylori
•common cause of [color=#ff6666]peptic ulcer disease
•tx: (cap) [color=#3366ff]clarithromycin, amoxicillin, ppi (proton pump inhibitor)
–[color=#009900]salmonella
•common cause of [color=#ff6666]diarrhea; some forms also cause [color=#ff6666]typhoid or sepsis
•[color=#3366ff]ciprofloxacin (rule out c.dif with any infectious diarrhea)
–[color=#009900]shigella
•causes [color=#ff6666]bloody, purulent diarrhea in nursing homes and preschools
•tx: [color=#3366ff]ciprofloxacin
–[color=#009900]vibrio cholera
•causes rice water diarrhea, with death from dehydration
•tx: [color=#3366ff]doxycycline, fluids and electrolytes
[color=#009900]–yersenia
•one form causes [color=#ff6666]diarrhea; another form causes [color=#ff6666]bubonic plague
•tx: [color=#3366ff]gentamicin
•gnr and sepsis: notes of interest
–many gnr have endotoxins, which are actually components of their cell wall
•when antibiotics begin their destruction, these toxins are released into the bloodstream in massive quantities, leading to sepsis (massive immune response) and eventually septic shock (low bp and organ dysfunction)
•for this reason, bacteremia (bugs in blood) with gnr is among the most serious of diseases, and should be treated aggresively in an icu
•with shock and 2 organs dysfunctioning the [color=#ff6666]mortality rate is over 40%; with each additional organ dysfunction add 15%
•[color=#ff6666]sepsis is the #1 killer in the icu, but is more preventable than you would think; the dirty source, is more often than not, indwelling catheters, so take extreme care with hygiene if you are icu bound!!!
– s/s: polyuria, dehydration, ab pain, fruity breath, ams, ↓ na/mg/phos, ↑k (↓ total body), + following:
• hyperglycemia (>250)
• metabolic acidosis (ph 20)
• ketonuria/ketonemia
– tx:
• iv [color=#3366ff]insulin bolus (0.1 unit/kg) then iv infusion with same amount per hr after making sure pt is not ↓ k
– continue until acidosis corrects then taper
• [color=#3366ff]ns immediately upon diagnosis
– switch to [color=#3366ff]d5ns when glucose
• why in the world would i give d5ns when a patient still has high glucose levels? the most important problem is the acidosis that is occurring. to reverse this we give insulin to drive glucose into the cell. remember that k rushes into the cell along with the glucose, and wherever k can go, h+ can go. since high levels of h+ in the blood is the cause of the acidosis, we give insulin to drive this h+ intercellularly, thereby reversing acidosis. we can't give insulin if the level of glucose is too low, so we give d5ns to keep levels around 250 so we can give insulin until the acidosis is gone.
– severe ↑ glucose, almost exclusively in type 2 diabetics
– similar to dka but usually have much higher glucose (>600) and no acidosis or ketonuria/ketonemia
– treat with [color=#3366ff]fluids and [color=#3366ff]low dose insulin infusion
– an important distinction is that dka usually occurs in type 1 diabetics, while hhns most often occurs in type 2 diabetics. remember this as it is a common question in the nclex world.
hypoglycemia:
– patho: when glucose drops to 80 = insulin levels ↓ ; 70 = glucagon ↑; 50 = epinephrine ↑ along with s/s such as sweaty, ↑bp, ↑hr, tremors; also around 50 cns s/s (drowsy, h/a, confused) begin
– note: s/s from epinephrine release are absent if pt is on a bb
– tx: if pt is alcoholic give[color=#3366ff]thiamine before any other treatment to prevent encephalopathy
• can eat = ↑ sugar food;
• can not eat = [color=#3366ff]½ - 2 amps d50 iv push; (glucagon alternative option if no iv access is available, however is of no use in prolonged hypoglycemia because stores of glycogen are depleted)
points to remember:
– for high sugar (dka, hhns) most of the signs and symptoms are from polyuria, so look for dehydration and electrolyte imbalances...remember high and dry
– for low sugar most of the signs and symptoms are from the release of epinephrine, so look for things that would happen when someone was high on adrenaline, such as hypertension, sweating, tachycardia and tremors.
– imperative that you can recognize the difference between these two, as you are almost guaranteed to see a question relating to this difference!
jadu1106
908 Posts
wow vadee, i am so amazed! thank you so much for posting all this information....acid/base is one of my weak areas, next to cardiac! :)