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Pharmacology Exam with Verified Solutions, Exams of Nursing

University of WestminsterNursing

A comprehensive study guide or exam preparation material covering various pharmacological concepts and principles. It delves into topics such as the impact of antibiotics on gut flora, drug-drug interactions, protein binding, volume of distribution, sepsis management, adrenergic receptor pharmacology, vasopressor and inotropic agents, and their mechanisms of action, pharmacokinetics, and adverse effects. Detailed explanations and verified solutions, making it a valuable resource for students or healthcare professionals seeking to enhance their understanding of clinical pharmacology. The breadth of topics covered and the level of detail suggest this document could be useful for university-level courses in pharmacology, nursing, or medicine.

Typology: Exams

2023/2024

Available from 10/14/2024

johnrays
johnrays 🇬🇧

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AACN Pharmacology EXAM with verified
solutions
GI flora changes from antibiotics - ANS 1. Decreased GI flora which produce Vit. K -
warfarin pts prone to bleeding
2. Decreased production of estrogen metabolites by gut flora - estrogen based
contraceptives less effective
3. MACROLIDES decrease amount of gut flora which metabolize Digoxin, therefore the
active concentration increases
Chelation of oral drugs - ANS 1. Cipro with antacids
2. Cholecystyramine (prevalite) with almost any other PO drug
3. Sucralfate with any other antacid - need AT LEAST 30 MIN between administration
Major binding proteins - ANS Alpha1-acid glycoprotein
Albumin
*Both decreased in critical illness
Protein bound drugs - ANS E.g. Warfarin - has very low free fraction
The more protein bound a drug is, the higher chance of adverse reactions and drug
interactions—changes in diet or health and other drugs competing for protein binding
sites alter free fraction
Drug with higher protein affinity will bind and other drug will have increased free fraction
- e.g. aspirin displacing warfarin
Poorly protein bound drugs - ANS Gentamicin - free fraction relatively independent of
protein
Volume of distribution - ANS The extent to which a drug moves out of intravascular
space into body tissues
(Lot of movement out = high volume of distribution)
Dependent upon lipid vs water solubility and protein binding
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AACN Pharmacology EXAM with verified

solutions

GI flora changes from antibiotics - ANS 1. Decreased GI flora which produce Vit. K - warfarin pts prone to bleeding

  1. Decreased production of estrogen metabolites by gut flora - estrogen based contraceptives less effective
  2. MACROLIDES decrease amount of gut flora which metabolize Digoxin, therefore the active concentration increases Chelation of oral drugs - ANS 1. Cipro with antacids
  3. Cholecystyramine (prevalite) with almost any other PO drug
  4. Sucralfate with any other antacid - need AT LEAST 30 MIN between administration Major binding proteins - ANS Alpha1-acid glycoprotein Albumin *Both decreased in critical illness Protein bound drugs - ANS E.g. Warfarin - has very low free fraction The more protein bound a drug is, the higher chance of adverse reactions and drug interactions—changes in diet or health and other drugs competing for protein binding sites alter free fraction Drug with higher protein affinity will bind and other drug will have increased free fraction
  • e.g. aspirin displacing warfarin Poorly protein bound drugs - ANS Gentamicin - free fraction relatively independent of protein Volume of distribution - ANS The extent to which a drug moves out of intravascular space into body tissues (Lot of movement out = high volume of distribution) Dependent upon lipid vs water solubility and protein binding

High Vd - ANS Poorly protein bound, lipid soluble Sepsis - ANS qSOFA score > -->higher is worse qSOFA (quick sequential organ failure assessment) - ANS respiratory rate > SBP </= GCS < Septic shock - ANS MAP <65, Lactic >2 despite adequate (30ml/kg NS) fluid boluses 3 hour surviving sepsis bundle - ANS - measure lactate, get BCs, hang ABX w/in 1hr of arrival

  • if lactate >4 or MAP <65, 30ml/kg fluid bolus 6 hour surviving sepsis bundle - ANS - pressors to maintain MAP >65 if unresponsive to fluid bolus
  • reassess volume status if MAP <65/lactate remain >
  • continue to remeasure lactate per protocol if initial elevated Hyperglycemia in sepsis - ANS - initiate insulin drip when two consecutive BS >
  • target BS <180, rather than lower levels
  • Patho: stress response causes increased glycogenolysis and hepatic gluconeogenesis. cytokine release causes insulin resistance. Adrenoreceptors - ANS Specific receptors throughout the body that are stimulated by or inhibit sympathomimetic activity
  • Alpha (respond to sympathomimetic activity - usu excitatory)
  • Beta (inhibit sympathomimetic activity - usu inhibitory) Alpha 1 stimulation - ANS **vasoconstriction therefore increased PVR/BP
  • also bladder contraction, pupil dilation alpha 2 stimulation - ANS inhibits norepi release therefore decreases sympathetic outflow and alpha 1 stimulation Beta 1 stimulation - ANS increased heart rate (aka positive chronotropy)

PD: A1, A2, & B1 receptor stimulation

  • vasocontrictor
  • +inotrope Dose range: stop at 10 to reeval, hard stop 30 mcg/min NE SEs - ANS - reflex bradycardia (increasing BP = STOP signal to coronary baroreceptor firing)
  • tachycardia (B1 stimulation)
  • ventricular dysrhythmias including PVCs
  • urinary retention vs AKI from renal aa constriction
  • restlessness, tremors, anxiety (think adrenergic neuro effects) NE doses >10mcg/min - ANS - evaluate for metabolic acidosis (severe acidosis will make pressors ineffective). treat appropriately if present
  • consider adding vasopression vs epi, steroids + eval for adrenal insufficiency
  • if still unstable, consider dobutamine infusion for inotropic effects (increased CO and tissue perfusion) Vasopressin MOA - ANS - synthetic ADH - secreted by posterior pit
  • V1 controls water reabsorption (aquaporin migration in DCT and collecting tubules)
  • V2 increases aa sm mm tone -->NOTE: only pressor that doesn't act on adrenergic receptors Vasopression - ANS - half life: 10-20 min -->LONGEST of all VPs!!
  • PK: not protein bound, high Vd to tissues, liver metab/renal elim
  • PD: VP1 &2 receptors cause increased SVR + increased preload from H2O retention renally
  • cannot be given PO - destroyed by stomach enzyme trypsin Vasopressin in septic shock - ANS - septic shock causes depletion in supply of stored vasopressin and also results in decreased ACTH stimulation, therefore decreased cortisol which also contributes to refractory hypotension, therefore, replacement dosed continuous infusion should be administered.
  • DOSE: 0.03 U/min per guidelines
  • range: 0.01-0.04 U/min Vasopressin SEs - ANS - decreased coronary perfusion
  • worsening chronic nephritis - contraindicated in these patients
  • volume overload - monitor CHF patients carefully Desmopressin (DDAVP) - ANS - primarily V2 ADH analog, so used for DI treatment
  • can be given orally Dopamine - ANS Dopamine renal dosing - ANS *does initially improve urine output 2/2 renal dopaminergic receptor activation *BUT does NOT clear metabolic toxins or preserve renal function. Epinephrine - ANS *second line for septic shock *first line for cardiac arrest. can be given in ETT. *used for positive chronotropic effects in patients who have non-cholinergic bradycardia, like neurogenic shock *causes hyperglycemia (stress response causing insulin resistance, glycogenolysis, and increased hepatic gluconeogenesis) and lactic acidosis from altered pyruvate metabolism (not hypoxia) Angiotensin II - ANS *giapreza *used for refractory hypotension in septic shock *places patient at high risk for venous and arterial thrombosis dobutamine - ANS *beta 1 agonist
  • inotropic agent, inc. contractility and CO, does NOT inc HR.
  • used in acute management of heart failure and myocardial dysfunction in septic shock. *doses >20mcg/kg/min assoc with tachyarrhythmia!! Sepsis induced myocardial dysfunction (SIMD) - ANS *occurs early - cytokines, endotoxins (PAMPS and DAMPS), nitric oxide dysfunction 2/2 endothelial dysfunction

aka membrane metallo-endopeptidase aka Neutral endopeptidase *MOA: inhibit neprilysin, which is an enzyme that catalyzes natriuretic peptide degradation, thereby allowing them to exert effects to reduce BP and SVR for much longer duration. *MUST NOT be given with ACE-Is -- in combo, are much more likely to cause angioedema because both inhibit renin, which causes increased bradykinin build up. Natriuretic Peptides (ANP and BNP) - ANS origin: atrial and ventricular myocytes, brain Target: Kidneys, Hypothalamus, adrenal gland Function: long-term regulation of sodium and water balance, blood volume and arterial pressure. There are two major pathways of natriuretic peptide actions: 1) direct arterial and venodilator effects, and 2) renal effects to decrease renin secretion and increase natriuresis and diuresis in K sparing manner. Calcium channel blockers - ANS - bind to L-type calcium channel on myocytes and vascular smooth muscle, which blocks calcium entry into cells, preventing firing (therefore, vasodilation and decreased chronotropy and inotropy result, as well as decreased dromotropy)

  • three types:
  1. dyhydropyridines - effect only vascular smooth muscle. end in "pine"
  2. nondyhydropyridines - verapamil (mostly myocardial) and dilt. (both myocardial and vascular) Nicardipine - ANS *hepatic metabolism, renal elimination *diphydropyridine--vascular only! *onset: 15 minutes *half-life: 8 hours *starting dose: 5mg/hr. *increase by 2.5 q15 min *SE: flushing, peripheral edema, asthenia (debility, fatigue, weakness), gingival hyperplasia, polyuria Nitroprusside (Nipride) - ANS *unlike organic nitrates, this nitrate preferentially arterially vasodilates vessels via triggering spontaneous release of nitric oxide, which decreases intracellular calcium release, calcium entry into cells, causes hyperpolarization of cells

via K+ channel activation, and activates myosin light chain phosphatase, which dephosphorylates myosin light chain, allowing relaxation *onset: instant *half life: 2 minutes *High Vd--distributes rapidly to tissues. *Eliminated as a thiocyanate/cyanide metabolite in urine, feces, and expelled air--takes 2 - 7 days to be completely eliminated. *CAN CAUSE CYANIDE TOXICITY if cont, high dose infusion >72h *do not use for >24-48h *Max dose: no more than 10mcg/kg/min for 10 min. Most maintenance doses are 3mcg/kg/min Cyanide toxicity - ANS *Possible SE of nitroprusside therapy. *likely to occur only if patient is on max dose for >72h. *S/S: AMS, GI complaints, dysrhythmias, sz, lactic acidosis Mannitol - ANS *PO only--doesn't cross GI epithelium *can be bolus or cont *Dosing:

  • 0.25-1g/kg over 30-60 min bolus
  • 0.25-0.5g/kg cont infusion *monitoring:
  • check serum OSM!!! hold for OSM >
  • electrolytes -->can cause low or high sodium and potassium
  • hold for hypotension *Warnings:
  • can cause rebound increased ICP ~12h post administration
  • give at rm temp thru inline filter to avoid infusing crystals -- great care if patient on therapeutic hypothermia Hypertonic saline - ANS *Osmotic diuresis which pulls fluid from the extravascular sites of swelling into the vessels for excretion renally *Dosing:
  • 0.5-1mg/kg/hr *Monitoring:

negative inotropes - ANS *CCBs *BB *lidocaine *quinidine *ABB (propranolol) Dobutamine - ANS *B1 and B2 agonist

  • positive inotrope (dose dependent increases)
  • vasodilation (B2 and increased CO outweighs A1 slight activity)
  • positive chronotropy <10mcg/kg/min *Half-life: 2 min *infusion: 5mcg/kg/min starting dose. maint 2.5-20mcg/kg/min *SEs: dysrhythmia (esp w/ preexisting myocardial ischemia), hypokalemia, n/v afib/atrial dysrhythmias - ANS *require testing for hyperthyroidism Loading dose - ANS the administration of a drug in sufficient quantity to promote more rapid absorption and distribution in tissue Bolus dose - ANS an amount of medication administered rapidly, or all at once, to decrease the response time or to be used as a loading dose prior to an infusion.