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65 Cards in this Set
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- Back
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Histamine
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Found in the CNS, the gastric mucosa, and other peripheral tissues
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Where highest concentration of histamine is found.
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Highest concentration of histamine is found in the storage granules of circulating basophils and mast cells throughout the body
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Histamine
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Found in the CNS, the gastric mucosa, and other peripheral tissues
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> 145 mmol/L raises osmotic gradient and causes water mov’t out of cells
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Hypernatremia
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Where highest concentration of histamine is found.
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Highest concentration of histamine is found in the storage granules of circulating basophils and mast cells throughout the body
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> 145 mmol/L raises osmotic gradient and causes water mov’t out of cells
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Hypernatremia
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Hypernatremia
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Causes:
Loss of water d/t fever, burns, infection, renal loss, GI loss Retention of Na d/t admin of hypertonic saline (HS) or any form of Na |
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Hypernatremia
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Causes:
Loss of water d/t fever, burns, infection, renal loss, GI loss Retention of Na d/t admin of hypertonic saline (HS) or any form of Na |
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Hypernatremia Treatment
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Administer free water orally or use D5W IV
If Na and H2O depleted use D5W ¼ NS or D5W ½ NS If pt is hypotensive due to vol. depletion use 0.9% NaCl to restore tissue perfusion |
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Hypernatremia Treatment
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Administer free water orally or use D5W IV
If Na and H2O depleted use D5W ¼ NS or D5W ½ NS If pt is hypotensive due to vol. depletion use 0.9% NaCl to restore tissue perfusion |
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Hyponatremia
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Hypo-osmolality causes fluid to shift into cells (Cellular overhydration)
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Symptoms:Hyponatremia
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E: Nausea, malaise < < HA, lethargy, obtunded
A: Seizure, coma (110-115) |
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Hyponatremia
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Hypo-osmolality causes fluid to shift into cells (Cellular overhydration)
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Symptoms:Hyponatremia
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E: Nausea, malaise < < HA, lethargy, obtunded
A: Seizure, coma (110-115) |
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Hyponatremia Causes:
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Sneaky – severe hyperlipidemia and hyperglycemia will cause hyponatremia
Loss of solute then replacing lost fluid with water (Vomiting/diarrhea/diuretics) Post-op admin of hypotonic fluids Vol. depletion + organ hypoperfusion = stimulation of ADH to increase H2O reabsorption Renal Failure (can’t dilute urine) and SIADH |
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Symptoms:Hyperkalemia
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enhanced by hypocalcemia hyponatremia, acidosis, or acute onset
Abnormal cardiac conduction; peaked narrow T waves (> 6 mmol/L) Muscle weakness (> 8 mmol/L) **watch hemolysis or serum levels rather than plasma levels |
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Causes: Hyperkalemia
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Increased intake
Reduced urinary excretion Kidney failure, intravascular vol. depletion, hyopaldosteronism, K+ sparing drugs K+ shift from IC to EC d/t Acidosis, insulin deficiency, beta adrenergic blockade, digoxin toxicity, rewarming after hypothermia, succinylcholine |
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Hyperkalemia Treatment:
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asymptomatic patients can just receive cation exchange resin (sodium polystyrene, Kayexalate®)
For EKG changes: Give 1 gram amp (10% 10ml Ca++ gluconate) IV over 5-10 min; may repeat Antagonizes effect of K+ in cardiac conduction cells; short lived; **don’t give if on digoxin!! -- can precipitate toxicity |
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Hyperkalemia Treatment:
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10 units reg insulin IV + 25-50 grams glucose (< 0.5-1.5 mmol/L in 1 hour)
Beta-2 adrenergic agonists – albuterol 10-20mg (4-8 neb amps) nebulized over 10 min (< 0.5-1.5 mmol/L) 1 amp (50meq) Sod Bicarb (best in acidosis, less so in renal failure) **follow with Kayexalate (15-30g q6h PO or enema), diuretics, or dialysis for persistent K+ lowering effect |
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Hypokalemia Symptoms:
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generally < 3.0 mmol/L
Muscle weakness EKG changes (flattened T or elevated U waves) Cardiac arrhythmias Digoxin toxicity despite normal dig level Rhabdomyolysis – dec. bloodflow to muscle |
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Hypokalemia Causes
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reduced intake seldom culprit
Increased K+ into cells Alkalosis, insulin or carbohydrate load, stress induced epinephrine release or beta agonist drugs (albuterol, dopamine, etc), hypothermia GI losses (vomiting, diarrhea, fistulas, enteral tube drainage) Increased urinary loss Hypomagnesemia |
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Hypokalemia Treatment
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treat underlying cause and:
Use KCL orally or IV (mix in normal saline!!) **must dilute (minimum 10meq KCL/50ml NS) Use 10meq KCL/100ml NS to avoid irritation Usually 10-20meq KCL/hr; make give up to 40meq/hr if life-threatening arrythmia 20meq/hr and > please monitor EKG |
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Magnesium
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2nd most prevelant IC cation after K+
Mag abnormalities strong linked to other lytes, esp. K+ Normal 0.7-1.0 mmol/L @ Trover 1.4-1.8 mEq/L or 0.85-1.15 mmol/L other places |
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Hypermagnesemia
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occurs with chronic kidney dz
S/S includes N/V, bradycardia, hypotension, heartblock, asystole, resp failure D/C all mag products Asymptomatic + good kidneys = 0.9% NS and loop diuretics Symptomatic = 1 gram Ca++ IV push and hemodialysis if needed |
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Hypomagnesemia
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Common in hospitalized patients
S/S = tetany, twitching, seizures, arrhythmias, hypertension Causes: Impaired intestinal absorption (colitis, diarrhea, low intake, hypokalemia, diuretics, alcoholics) Treatment: PO supplementation – limited by diarrhea; IV – can give 1 gram over 15-20 min but try to give 1 gram per hour (better retention); cut dose in half for renal patients |
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Initiation of treatment prior to determination of a firm diagnosis
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Empiric therapy
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Organism and susceptibilities are known
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Definitive therapy
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Prevent initial or recurrent infection
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Prophylaxis
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Lowest concentration of drug that prevents visible bacterial growth
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Minimum Inhibitory Concentration (MIC)
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Causes bacterial death
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Bactericidal
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Inhibits growth
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Bacteriostatic
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Beta-lactams
Vancomycin |
Time-Dependent (with minimal or no PAE)
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Aminoglycosides
Daptomycin Fluoroquinolones Metronidazole Azithromycin |
Concentration-Dependent (with PAE)
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Vancomycin, Bacitracin, Penicillins, Cephalosporins
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Cell Wall Integrity
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B-lactamases
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Cell Wall Synthesis
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Metronidazole, Quinolones
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DNA Synthesis
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Rifampin
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RNA Polymerase
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Protein Synthesis
30 S Inhibitors |
Tetracyclines, Streptomycin, Kanamycin
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Erythromycin, Choramphenicol, Clindamycin
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Protein Synthesis
50 S Inhibitors: |
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Polymyxins
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Phospholipid Membranes
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MOA: All inhibit cell wall synthesis
Bactericidal (exception: Enterococcus) Time-dependent killers Short t1/2 Primarily renally eliminated (exceptions: nafcillin, oxacillin, ceftriaxone - Rocephin®) Resistance: β-lactamase degradation |
B-Lactam Characteristics
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Confirm presence of infection
Identify the pathogen Selective empiric therapy based on host and drug factors Site of Infection Route & Duration of treatment **Risk of development of resistance Cost (Efficacy and toxicity may influence) |
How do you determine which antibiotic to use?
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Inhibit bacterial topoisomerases which are necessary for DNA synthesis.
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Flouroquinolones MOA
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Inhibits protein synthesis by reversibly binding to the 50S ribosomal subunit
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Macrolides MOA
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Inhibition of protein synthesis by IRREVERSIBLY binding to 30S ribosomes resulting in a defective bacterial cell membrane
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Aminoglycosides MOA
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Inhibits bacterial cell wall synthesis at final stage of peptidoglycan
Bactericidal |
Vancomycin MOA
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Binds to bacterial membranes and causes rapid depolarization of the membrane potential, inhibiting synthesis of protein, DNA, RNA and protein.
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Daptomycin MOA
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Reversibly binds to 50S ribosomal subunits inhibiting bacterial protein synthesis
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Clindamycin MOA
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After complex reduction reactions, causes DNA to lose helical structure and results in inhibition of protein synthesis
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Metrondazole MOA
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Inhibits dihydropteroate synthase – inhibits incorporation of p-aminobenzoic acid (PABA) into dihydrofolic acid
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TMP/SMX (bactrim) MOA
SMX |
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Inhibits dihydrofolate reductase – prevents reduction of dihydrofolate to tetrahydrofolate
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TMP/SMX (bactrim) MOATMP
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Clarithromycin (Biaxin) & azithromycin (Zithromax):
Broader spectrum of activity Improved PK properties: Better bioavailability Better tissue penetration Prolonged half-lives Improved tolerability |
advantages of the newer marcolides over erythromycin
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Normal 2.4-4.4 mg/dl
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Phosphorus
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Typically seen in renal failure and hypoparathyroidism
S/S = hypocalcemia, EKG changes, paresthesias, vascular calcifications Treatment: Phosphate binders calcium carbonate (acetate) or dialysis |
Hyperphosphatemia
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S/S = tissue hypoxia, confusion & delirium, seizure, coma, resp failure, heart failure
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Hypophosphatemia S/S
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increased renal elimination, chronic malnutrition patients “refeeding syndrome”, respiratory alkalosis, treatment of DKA – phos shifts into IC compartment
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Hypophosphatemia causes
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neutraphos oral packets, IV Na or K phos
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Hypophosphatemia treatment
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serum 8.4-10.2 mg/dl
ionized 4.48-4.92 mg/dl or 1.1-1.3 mmol/L 1% EC and 99% bone |
Calcium
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Approx. half of ? in the EC compartment is bound to plasma proteins (albumin)
Must correct for low albumin |
Calcium
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Most commonly found in malignancy and hyperparathyroidism – watch EKG changes and renal damage
Ionized Ca++ can be increased with acidosis |
Hypercalcemia
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can be increased with acidosis
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Ionized Ca++
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For malignancy give IV saline hydration, a bisphosphonate (Pamidronate IV), and possibly a diuretic
Some patients respond to calcitonin Corticosteroids less predictable – take a couple weeks to lower calcium Lower calcium slowly over 24-48 hours |
Hypercalcemia
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tetany, muscles spasms, hypoactive reflexes, anxiety, hallucinations, lethargy, hypotension, seizures
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Hypocalcemia s/s
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CKD, hypoparathyroidism, Vit D defficiency, alcoholism, hyperphosphatemia, large amounts of blood products, Ionized Ca++ can be low with alkalosis
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Hypocalcemia causes
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generally requires 2-4 grams of oral calcium per day along with Vit D supplementation
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Asymptomatic hypocalcemia
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