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BPH and more

QuestionAnswer
testosterone replacement can cause or exacerbate BPH
a-agonists (pseudoephedrine) can cause or exacerbate BPH
beta agonists (terbutafine) can cause or exacerbate BPH
medications with anticholinergic properties can cause or exacerbate BPH
antihistamines can cause or exacerbate BPH
tricyclic antidepressants can cause or exacerbate BPH
antispasmodics with anticholinergic properties can cause or exacerbate BPH
parkinson's disease medications with anticholinergic properties can cause or exacerbate BPH
diuretics can cause or exacerbate BPH
PSA >1.4 BPH
AUA <7 mild
AUA 8-19 moderate
AUA >20 severe
if AUA <8 or >8 but no symptoms watchful waiting - reevaluate annually - decrease fluid intake at night, caffeine/alcohol, avoid medications that can exacerbate symptoms
if AUA >8 with bothersome, moderate to severe symptoms (normal prostate) alpha blockers
alpha blockers -osin
uroxatral alfuzosin
cardura doxazosin
rapaflo silodosin
flomax tamsulosin
hytrin terazosin
intraoperative floppy iris syndrome (IFIS) occurs more often in patients on alpha blocker who get cataract surgery
drugs associated with intraoperative floppy iris syndrome (IFIS) doxazosin, silodosin, tamsulosin
drugs not indicated for BPH prazosin, phenoxybenzamine
if AUA >8 with bothersome, moderate to severe symptoms (large prostate) a blocker or 5-ARI or both
if AUA >8 with bothersome, moderate to severe symptoms (with ED) a blocker or PDE-5 inh or both
if AUA >8 with bothersome, moderate to severe symptoms (predominantly irritative symptoms) a blocker + anti-ach or a blocker + b3 agonist
men with LUTS secondary to BPH who have prostate enlargement 5-alpha reductase inhibitor
avodart dutasteride
proscar finasteride
5-alpha reductase inhibitor -steride
qualifications (just have to have one) >30g prostate measured ultrasound PSA >1.5 "large" finding in DRE assessment
if men have LUTS secondary to BPH without elevate PRV and when LUTS is a PREDOMINANTLY IRRITATIVE (caution in patients with PRV >250-300mL) anticholinergic agents
anticholinergic notes tolterodine best studied but can use all antimuscarinics used in overactive bladder monitor 4-6 weeks after starting mirabegron (B3 agonist) as an alternative
no guidelines ED and BPH exist PDE-5 inhibitors
DDI with alpha blockers PDE-5 inhibitors
tadalafil the ONLY fda-approved PDE-5 inhibitor for BPH
Tadalafil dosing 5 mg PO daily
cialis tadalafil
PDE-5 inhibitors -afil
herbals such as saw palmetto, stinging nettle, star grass, pumpkin seed, african plum Guidelines: No complimentary and alternative medicine is recommended for the management of LUTS secondary to BPH
surgical options Consider an option for moderate to severe BPH May be necessary if patient experiencing BPH related complications Most fail medication before proceeding with surgery
a blockers onset fast (1-6 weeks)
5-ARIs onset very slow (6-12 months)
a blockers 2nd gen doxazosin (cardura), terazosin (hytrin), alfuzosin (uroxatral)
a blockers 3rd gen (a-1a) tamsulosin (flomax), silodosin (rapaflo)
a blocker clinical efficacy AUA-SI Change: improve AUA-SI 30-40% (often 3-6 points) Urine Flow: ↑ flow rate 2-3 mL/s in most patients Prostate Size: no effect Other: reduces post-void residual (PVR) urine volume
5-ARIs dutasteride (avodart), finasteride (proscar)
5-ARIs clinical efficacy AUA-SI Change: improve AUA-SI ~2-4 points Urine Flow: ↑ flow rate 1.6-2 mL/s Prostate Size: decrease size by 25% Other: decrease risk of AUR and need for surgery (↓ progression)
PDE-5 inhibitors tadalafil (cilais)
PDE-5 inhibitors clinical efficacy AUA-SI Change: improve AUA-SI ~2-4 points Urine Flow: minimal increase Prostate Size: no effect Other: tadalafil is only PDE-5 inhibitor approved for BPH (2011)
PDE-5 inhibitors onset moderate (4 weeks)
anticholinergic agents tolterodine (detrol LA)
anticholinergic agents onset fast (1-2 weeks)
anticholinergic agents clinical efficacy Efficacious at decreasing irritative urinary symptoms (urinary frequency, urgency, and nocturia) Avoid with ↑ post-void residual (>250mL) may ↑ urinary retention
Likely all OAB anticholinergic agents effective Tolterodine, oxybutynin, darifenacin, solifenacin, fesoterodine, trospium
β3-agonists mirabegron (myrbetriq)
β3-agonists onset moderate (2-8 weeks)
β3-agonists clinical efficacy Efficacious at decreasing irritative urinary symptoms Similar efficacy to anticholinergics (better tolerated) Relaxes detrusor muscle (contracts bladder) Does not inhibit voiding, ↓ urine flow rate, or ↑ PVR
a blockers 2nd gen side effects First-dose syncope Orthostasis Dizziness IFIS (rare)
a blockers 2nd gen other Start low, go slow ↑ dose, ↑ efficacy, ↑ BP effects Take at bedtime Monitor BP (esp. if on anti-HTN meds)
3rd gen a blockers (plus alfuzosin) side effects Ejaculatory dysfunction IFIS (rare)
3rd gen a blockers (plus alfuzosin) other Alfuzosin – uroselective at usual doses ↓ BP effects vs. 2nd generation Take anytime during day Jalyn (dutasteride 0.5mg + tamsulosin 0.4mg combination capsule)
PDE-5 inhibitors side effects Headache Flushing Dyspepsia
PDE-5 inhibitors other Can be used with or without ED Caution with PDE-5 inhibitors and alpha blockers that can drop BP Only use tadalafil 5mg po daily
5-ARIs side effects ↓ libido Erectile dysfunction Ejaculatory dysfunction Gynecomastia (rare) ED may be secondary to nitric oxide synthase inhibition
5-ARIs other Sexual side effects may be significant and effect use in sexually-active men Pregnancy category X (RPh of childbearing age  gloves)
anticholinergic side effects Anticholinergic side effects (anti-SLUD)
anticholinergic other Consider total anticholinergic burden Urinary retention tolterodine = placebo in trials
B3-agonists side effects Hypertension
B3-agonists other Use for irritative symptoms when anticholinergics not tolerated expensive!
functional incontinence cant get to the restroom on time (elderly) Spinal problems
Medications that can affect bladder function Allergy medications Analgesics/sedatives Anticholinergic Diuretics SNRI Muscle relaxants
urgency incontinence Sudden or compelling urge to pass urine that is difficult to defer Overactive bladder: syndrome characterized by urinary urgency, frequency, and nocturia, with or without incontinence Associated with detrusor muscle overactivity
the ONLY UI we have meds for urgency incontinence
antimuscarinics Often used as initial pharmacotherapy Start low and go slow! ER preferred over IR Have anticholinergic effects that may limit tolerability and dose escalation Not one is better than another in the class in regards to efficacy
antimuscarinics CI narrow angle glaucoma
antimuscarinics caution Caution with dementia, decreased GI motility, urinary retention, tachyarrhythmias (atrial fibrillation)
oxybutynin most anticholinergic
trospium least anticholinergic
expensive but has least side effects trospium
cheap but most side effcts oxybutynin
OTC patch option oxybutynin
QTC prolongation solifenacin (vesicare)
QTC prolongation tolterodine (detrol, detrol LA)
interaction with 3A4 inhibitors darifenancin (enablex)
interaction with 3A4 inhibitors fesoterodine (toviaz)
interaction with 3A4 inhibitors solifenacin (vesicare)
interaction with 3A4 inhibitors tolterodine (detrol, detrol LA)
B3-agonist for UI Can be used in initial therapy or in patients that do not tolerate antimuscarinics Combination of antimuscarinic + beta3 agonist may be used
more B3-agonists mirabegron, vibegron (gemtesa)
stress incontinence Involuntary leakage of urine with increases in intra-abdominal pressure Sneezing, coughing, laughing, exercising
stress incontinence treatments 1) lifestyle modifications + pelvic floor exercises (Kegals) 2) support devices 3) surgery
stress incontinence treatments NON-FDA approved Topical vaginal estrogen - menopause Duloxetine (Cymbalta)
stress incontinence treatments lifestyle modifications Recommended for most types of incontinences Weight loss Dietary changes Smoking cessation Bladder training (most effective for urgency incontinence) Exercises: pelvic floor (Kegel) most effective for stress incontinence
overflow incontinence Continuous urinary leakage or dribbling in the setting of incomplete bladder emptying Caused by detrusor underactivity or bladder outlet obstruction
overflow incontinence treatments Treatment depends on cause: Detrusor muscle underactivity not a lot of treatment options Bladder outlet obstruction  urologist
Urinary Incontinence in men treat BPH Lifestyle modifications preferred like women BPH + UI Alpha blockers first line If irritative symptoms persist add antimuscarinic or beta3 agonist
vibegron DI Vibegron is a better substrate for the PGP – outcompetes digoxin – digoxin goes into blood increases cmax and auc
tolterodine metabolism 2D6 (3A4 in 2D6 poor metabolizers)
tadalafil MOA MOA not completely understood Inhibits phosphodiesterase type 5, increasing cGMP levels in prostate, urethra, bladder, and pelvic blood vessels This relaxes smooth muscles of intrinsic urethral sphincter and in prostate
a-adrenergic antagonists Relax intrinsic urethral sphincter and prostatic smooth muscle Do not reduce prostate size Do not affect prostate specific antigen (PSA)
Drugs Relaxing Prostatic Smooth Muscle α1-Adrenergic antagonists Phosphodiesterase 5 inhibitors
postsynaptic 2nd gen
prostatic 3rd gen
dutasteride nonselective - type I and II
finasteride selective - type II
Drugs Reducing Prostate Enlargement 5a-reducatase inhibitors
static factor enlargement
dynamic factor smooth muscle contraction
as men age Intracellular levels of DHT in prostate remain constant with aging (due to 5a reductase) estrogen converts
Which a1-adrenergic antagonists have cardiovascular side effects? Terazosin, doxazosin
Which a1-adrenergic antagonist is uroselective? Alfuzosin
Which has a potential for a drug allergy? Tamsulosin (sulfonamide)
Which quinazoline derivative has a rotatable propylenediamine group? Alfuzosin
Which ones are the a1A subtype? Tamsulosin and silodosin
5a reductase inhibitor process? Irreversible modification of 5 a reductase
Which 5a reductase inhibitor is non selective? Dutasteride (type I and II)
Which 5a reductase inhibitor has a higher logP? Dutasteride
Which 5a reductase is more potent dutasteride
Which of the following drugs has CYP3A4 metabolism? (like a select all) Doxazosin, alfuzosin, tamsulosin, silodosin, finasteride, dutasteride
Which anticholinergic agent has a patch formulation that bypasses first pass hepatic and gut metabolism? Oxybutynin
The immediate release formulation of Oxybutynin undergoes extensive first pass metabolism to be activated into this metabolite? DEO (N-desethyloxybutynin)
Which anticholinergic does not pass through the BBB? Trospium Chloride
Why does trospium chloride not pass through the BBB? The quaternary amine
Which anticholinergic agent is excreted through active tubular secretion (and can lead to a DDI)? Trospium chloride
Which anticholinergic agent should the dose be adjusted for severe renal impairment? Trospium chloride
Which anticholinergic agent is metabolized by estereases (no CYP enzymes)? Trospium chloride
In poor 2D6 metabolizers, the metabolism of detrol occurs by? CYP3A4
In Metabolism of Detrol through the CYP3A4 pathway what type of reaction does the drug undergo? N dealkylation and then further goes through hydroxylation
In Metabolism of Detrol through the CYP2D6 pathway what type of reaction does the drug undergo? Oxidation reaction
Which anticholinergic is classified as a Prodrug? Fesoterodine fumarate (Toviaz)
What is a prodrug? Inactive drug that is metabolized into an active metabolite
What is fesoterodine fumarate metabolized into? 5-hydroxymethyl tolterodine
What is fesoterodine fumarate activated by? Plasma esterases
Something about solifenacin half life? Its long (55 hr)
Which anticholinergic has an Oral bioavailability of 15-25%? Darifenacin
Finasteride and Dutasteride are both known as what kind of chemical structure? Azasteroid
As men age testosterone ----- and estrogen ----- and intracellular DHT in prostate -----. Decreases, increases, remains constant
What is responsible for later growth in men that causes BPH? DHT
Which is true about estrogen? Stimulates stromal tissues of prostate May induce androgen receptors
How much more potent is DHT to testosterone? 10x
What is a marker for prostate cancer? PSA >4
What is a static factor? Prostate enlargement
What is a dynamic factor? Contraction of prostate around urethra
Which of the following class of medication may exacerbate BPH symptoms? Testosterone replacement a-Adrenergic agonists Anticholinergics Diuretics
Which class of medications reduce serum PSA levels by 50%? 5-a Reductase inhibitors
What are the adverse effects of 5a-reductase inhibitors ED and nitric oxide synthase inhibition
Which drugs relax prostatic smooth muscle? a1 - adrenergic antagonists PDE5 inhibitors
Which drugs reduce prostate enlargement? 5a reductase inhibitors like finasteride and dutasteride
Which drugs are 2nd gen postsynaptic a adrenergic antagonists and can cause cardiovascular side effects? doxazosin and terazosin
Silodosin and tamsulosin are? 3rd gen prostatic a1A adrenergic antagonists
Which type of drugs do not reduce prostate size and do not affect PSA? A1 adrenergic antagonists
What are the adverse effects of Terazosin and doxazosin? First-dose syncope, orthostatic hypotension, and dizziness
____ and _____ often occur together BPH, ED
Which part of the bladder is voluntary? External urethral sphincter
What is the term for when the detrusor muscle is overactive and contracts inappropriately during filling? Bladder over activity
What is compromised during stress urinary incontinence? Urethral sphincter
What is overflow incontinence? Urethral overactivity- resistance to urine flow during urination Bladder under activity- detrusor muscle has weakened
What drugs are used for overactive bladder? Anticholinergics, Beta 3 adrenergic agonist, TCAs, topical estrogen
How do anticholinergics help with overactive bladder? Antagonize muscarinic cholinergic receptors to prevent detrusor muscle contractions Enhances bladder storage and relieves UI symptoms
Which of the following are Nonspecific muscarinic receptor antagonists? Oxybutynin Trospium
Which drugs have greater selectivity for M3 receptors than oxybutynin and trospium? Solifenacin and Darifenacin
What is tolterodine metabolized to? Active 5-hydroxymethyl metabolite (DD01)
What drug has a major DI with Vibegron? Digoxin
What is the TCA mentioned for UI Imipramine
What class is imipramine? SNRI TCA
What do the anticholinergic properties of Imipramine help with? Over active bladder
What does the SNRI portion of imipramine help with? Stress incontinence
What are the SSNRIs for stress UI? Duloxetine and Venlafaxine
What is topical estrogen used for? Stress UI
normal urine output 0.5-1.0 mL/kg/hr
Non-oliguria >500 mL/day
oliguria <500 ml/day
anuria <50-100 ml/day
AKI ↑ SCr by > 0.3 mg/dL within 48 hours ↑ SCr to > 1.5 x baseline within 7 days Urine volume < 0.5 mL/kg/hr x 6-12 hours
R SCr 1.5 – 1.9 x baseline GFR ↓ by 25% - 49% UO < 0.5 mL/kg/hr x 6-12 hours
I 2.0 – 2.9 x baseline GFR ↓ by 50% - 74% < 0.5 mL/kg/hr x > 12 hours
F > 3.0 x baseline OR GFR ↓ by > 75% OR > 4 mg/dL with acute ↑ > 0.5 mg/dL < 0.3 mL/kg/hr x > 24 hours OR Anuria x > 12 hours
L complete loss of kidney function > 4 weeks
E ESRD (> 3 months)
prerenal AKI Volume Depletion Dehydration Hemorrhage Gastrointestinal losses Arterial Occlusion/Stenosis Renal artery stenosis ↓ Effective Blood Volume Sepsis Heart Failure Valvular abnormalities Liver cirrhosis ACEIs/ARBs, NSAIDS
NSAID and ACE/ARB effects Ace inhibitors/arbs blocks Ang II – no constriction in the efferent arteriole NSAIDS block this PG and there will not be vasodialation – decreased perfusion
acute interstitial nephritis Most often caused by drugs/infections *NSAIDs *Beta-lactam antibiotics (penicillins, cephalosporins) *Sulfonamides (trimethoprim-sulfamethoxazole, loop/thiazide diuretics) *Proton pump inhibitors
acute tubular necrosis Aminoglycosides (gentamicin) Amphotericin B (antifungal) Cisplatin (chemo/cancer) Foscarnet (antiviral) Radiocontrast agents Vancomycin (MRSA)
postrenal AKI obsrtuctions Anticholinergic medications (anti-dumbelss) Crystal deposition (acyclovir (IV), indinavir)
fena <1 - prerenal >2 - ATN
use feurea when patient on diuretics
indications for acute hemodialysis metabolic acidosis, hperkalemia, toxification, overload, symptomatic uremia
ethacrynic acid most ototoxic - use if allergic to other loops
F 40 B 1 T 20 IV to oral furosemide 1:2
maximal ceiling dose for loops (IV blous) 200 mg fursosemide
diuretic combo therapy loop + metolazone
aminoglycoside induced nephrotoxicity prevention Avoid when possible and use for shortest necessary time when not possible to avoid Dose based on therapeutic drug monitoring (____TDM____): Monitor peaks and troughs Consider extended-interval dosing
amphotericin b prevention Avoid when possible and use _lipid_ formulations when not possible to avoid Correct electrolyte abnormalities Hydration with 0.9% NaCl prior to infusion then daily
cisplatin prevention Consider alternatives (i.e. carboplatin) if possible Consider addition of ___amifostine___ (cytoprotective inorganic phosphate) in high-risk patients Correct electrolyte abnormalities Hydration with 0.9% NaCl 12-24 hours prior to infusion x 2-3 days
vancomycin prevention Dose based on ___weight__________ , renal function, and therapeutic drug monitoring (TDM) Monitor vancomycin _____trough________ levels or AUC depending on institution protocol
prevention of CIN Use hydration to prevent CIN in high-risk patients 0.9% NaCl 1.0 – 1.5 mL/kg/hr 3-12 hours before __and___ 6-12 hours after contrast
calcium Normal serum Ca 8.0-10.4 mg/dL (total calcium) Ionized (free) Ca: 4.25-5.25mg/dL
calcium albumin ALWAYS correct total calcium for albumin Corrected calcium = calcium + 0.8 (4 – albumin) 
hypocalcemia Bisphosphonates Cinacalcet Loop diuretics
hypocalcemia treatment PO vs IV IV if symptomatic or corrected Ca ≤7.5 mg/dL (ionized ≤3mg/dL) Do not give >60mg of elemental Ca per minute --> risk of cardiac arrhythmias  Limit 500-600mg elemental Ca per dose to maximize absorption CONSTIPATION
hypercalcemia Lithium Thiazide diuretics
hypercalcemia treatment NS 3-6 L over 24 hours ± loop diuretics (if volume overload occurring due to aggressive hydration) Calcitonin (IV) Bisphosphonates (zoledronic acid or pamidronate)
calcitonin after 48 hrs tachyphylaxis
Denosumab (Xgeva)- Hypercalcemia of malignancy Option to treat hypercalcemia that is refractory to zolendronic acid or when bisphosphonates are contraindicated due to renal function
hypomagnesium Loop diuretics Amphotericin B Aminoglycosides Calcineurin inhibitors Digoxin Cisplatin
best friends mg, ca, k
hypomagnesium treatment PO magnesium (one study showed doses increased serum Mg levels on median of 0.1mg/dL) Mild-moderate Dose limiting effect- DIARRHEA
hypomagnesium treatment IV 2g IV increases serum Mg 0.2mg/dL
mg monitoring Mild-moderate: within 24 hours Severe- several hours after IV infusion (takes time to distribute to tissues)
isoosmolar 275-290 mOsm/kg
isotonic crystalloids Normal Saline-0.9% NaCl (NS) Lactated Ringer (LR) (balanced crystalloid) Plasmalyte or Normosol (balanced crystalloid)
hypotonic crystalloids Dextrose 5% in water (D5W) (free water) ½ Normal Saline-0.45% NaCl (1/2 NS)
hypertonic crystalloids Hypertonic Saline- generally 3% NaCl (red flag drug!)
colloids Albumin (5% or 25%) Packed Red Blood Cells (pRBC) Dextran Hetastarch
normal sline Commonly used for fluid resuscitation (replenishing fluid in vasculature
LR Most similar to blood plasma concentration Commonly used in trauma or burns
1/2 NS Hypernatremia with hypovolemia
3% Sodium chloride (HIGH ALERT MEDICATION) Critical care medication General use: Severe hyponatremia with neurological symptoms; traumatic brain injury (used to shrink the swelling from this injury)
NS 154 Na
4-2-1 1st 10 kg 4ml/kg/hr 2md 10 kg 2ml/kg/hr >20 1ml/kg/hr
100-50-20 100 ml/kg/day 50 ml/kg/day 20 ml/kg/day
Na 135-145
K 3.5-5.0
Cl 97-107
BUN 5-20
HCO3 23-29
SCr 0.8-1.2
Ca 8-10.4
Mg 1.5-2.4
PO4 2.5-4.5
WBC 5-10x10^3
Plt 150-400x10^3
Hgb F 12-16 M 14-18
Hct F 36-46 M 41-53
fluid loss treamtnet Treatment: Replace fluid (~1kg loss= 1L fluid replaced)
signs of excess fliud peripheral edema, JVD, pulmonary edema
hypokalemic goal Goal: >3.5 mEq/L but PREFER >4 mEq/L in cardiac patients and ICU patients
hypokalemic treatment replace Mg KCl
hypokalemic PO Max oral doses should be 60mEq (ideally 40 mEq max) per dose Can cause nausea/vomiting (especially if doses >40mEq at a time)
hypokalemic IV peripheral - 10 mEq/hr central w ekg - 20-40 mEq/hr
(K) For every 10mEq given, serum K will increase by ~0.1
renal impairment K generally decrease dose by 50%
hyperkalemia RAAS-active drugs (ACE, ARB) K+ sparing diuretics (spironolactone) NSAIDs Cyclosporine Trimethoprim-sulfamethoxazole (Bactrim) Heparins
Calcium gluconate Does NOT affect K levels in the body Purpose: normalize EKG Do NOT recommend if no EKG changes present Dose: 1 g IV x1 May repeat if necessary Monitor EKG
Calcium chloride is an option NOT preferred due to increase tissue damage in peripheral line
shifts K intracellulary Regular insulin albuterol sodium bicarbonate (only acidosis)
eliminates k loop diuretics, sod poly sul, patiromer, sod zirc cyclo
regular insulin 10 units
albuterol 20 mg in 4 ml NS
symptomatic hypernatremia GOAL:  Na by 0.5 mEq/L/hr or MAX of 12 mEq/L/day if CHRONIC hypernatremia GOAL:  Na by 1-2 mEq/L/hr or MAX of 12 mEq/L/day for ACUTE hypernatremia MAXIMUM correction in 24 hours: 8-12 mEq/L
TBW (female) = 0.5 L/kg x weight in kg
TBW (men) = 0.6 L/kg x weight in kg
free water deficit in liter TBW x (serum Na/140 - 1)
calculate how much to give in 24 hrs = water deficit x goal change in Na / (serum Na-140)
Hyperglycemia-induced hyponatremia (isotonic or hypertonic) corrected serum Na = measured Na + 1.6 (glucose -100 / 100)
SIADH Antidepressants Anticonvulsants Antipsychotics Chemotherapy Vasopressin analogs
calculate sodium deficit = TBW x (desired serum Na - measured serum Na)
estimate change in serum sodium from fluid = Naiv - Nas / TBW+1
Rapid increase in serum sodium  acute decrease in brain cell volume ODS
vaptans hepatotoxic, CI in hypovolemic hyponatremia
hypophosphatemia Insulin Antacids
fleet phospho soda (sodium phosphate solution) BBW kidneys
phosphate treatment 15mmol phosphate in 250mL D5W or NS over 3 hours May increase phosphate level by 0.5-0.8 mg/dL
pH 7.4 (7.35-7.45)
pCO2 35-45 mmHg
pO2 80-100 mmHg
HCO3 in blood gas 22-28 mEq/L
anion gap metabolic acidosis (agma) anion gap >12
anion gap metabolic acidosis (agma) mudpiles metformin, methanol, uremia, DKA, prop glycol, infection, lactic acidosis, ethylene glycol, salislyates
non anion gap metabolic acidosis (nagma) anion gap <12
non anion gap metabolic acidosis (nagma) usedcrap uterosigmoid, small bowel fistula, extra chloride, diarheea, carbonic anhydrase inhibitors, RTA, adrenal insuff, pancreatic fistula
respiratory acidosis cans CNS depressants (narcotics), airway obstruct, neuromuscular, sevevre pnemonua
metabolic alkalosis cleverpd contraction, licorice, endocrine, vomiting, axcess alkali, refeeding, posthypercapnia, diuretics
resp alkalosis champs CNS disease, hypoxia, anxity, mech vent, progesterone, salicylates
symptoms alkosis hypoven, hypokalemic
calculate anion gap (normal <12) AG= Na+-Cl--HCO3- Corrected AG= every 1 g/dL decrease in albumin (normal=4), add 2.5 to AG
ph <7.4 acidemia
ph>7.4 alkemia
resp alk low paco2
meta alk high hco3
Check for compensation Winter’s formula for metabolic acidosis Expected pCO2 = 1.5 (HCO3-) + 8 (± 2) Expected ↑ in pCO2 with metabolic alkalosis Expected ↑ in pCO2 = 0.75 (patient HCO3-  normal HCO3-) + 40
if agma check corrects hco3 Corrected HCO3- = patient’s HCO3- + (patient’s AG  normal AG)
For rise in AG by 1 corresponding decrease of HCO3 by 1 mEq/L
If calculated HCO3 is not in the reference range (22-28 mEq/L)  coexisting metabolic disturbance If > 28mEq/L, indicates corresponding metabolic alkalosis If < 22mEq/L, indicates a non-anion gap metabolic acidosis
Created by: Urmeme
 

 



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