Patho Final

Final Blueprint- Remember with the drugs review use, MOA, Class, major adverse effects ,
contraindications, and patient teaching
I would use the powerpoints and your notes to review.
Unit 1= Chapter 1,2, and 3
Types of drug classifications

By structure- pharmacological structure

MOA

Therapeutic classification- based on therapeutic use

Prototype Drug- well-understood drug model with which other drugs in its class are compared.
Pharmacokinetics- know what each is and what factors can influence them

 Absorption- movement of a drug from its site of administration into the bloodstream for distribution to the tissues (influenced by bioavailability)

Distribution- transport of a drug by the bloodstream to its site of action (influenced by amount of blood supply to an area * extensive blood supply= fast distribution)

Metabolism- biochemical alteration of a drug to an inactive metabolite, a more soluble compound

excretion- elimination of drugs from the body (influenced by half-life of the drug * the greater the half life the longer it takes to excrete)
Enteric and coated tabs and how it effects drug administration

Enteric- prevents delivery of drug in the stomach but permits release into the small intestine
Routes of drugs

Enteral- Oral, NG, Gtubes
•             Tablets- Oral disintegrating tablets, Enteric Coated, Sustained release
•             Sublingual and Buccal
•             Topical (and transdermal patches)
•             Ophthalmic
•             Otic
•             Nasal
•             Vaginal and Rectal
•             Intradermal
•             Subcutaneous
•             Intramuscular
•             Intravenous
First pass effect- what it is and how different drug routes are not affected by the first pass effect.

A drug that is absorbed from the intestine must first pass through the
liver before it reaches the systemic circulation.

Drug is absorbed, Drug enters hepatic circulation, goes to liver. Drug is metabolized to inactive form. Drug conjugates and leaves liver. Drug is distributed to general circulation Many drugs are rendered inactive by first-pass effect.

*Drugs that absorb directly into systemic circulation avoid first-pass effect (Suppository, IV, IM, inhalation, transdermal, sublingual)

Review ½ life- length of time needed to decrease drug plasma concentration by one half

What is purpose of peak and trough and when are they drawn, and reason why it is needed in
certain drugs such as Vancomycin and Gentamycin

Peak- highest blood level, 1-several hours after drug is administered

Trough- lowest blood level- immediately before next dose

*Needed for certain drugs to avoid toxicity
Therapeutic index

Ratio compares blood concentration at which a drug becomes toxic and concentration at which a drug is effective. Very narrow
Therapeutic effect vs adverse effect

Desirable or intended effects of a medication

Undesirable effects that are a direct response to one or more drugs
Types of allergic reactions and clinical manifestations

Allergic reactions- acquired hyper response of body defenses to a foreign substance

Anaphylaxis- severe type of allergic reaction, can lead to life threatening shock

Signs and Symptoms- Rash, edema, runny nose, reddened eyes with tearing
Rights of medicine

Right drug
•             Right dose
•             Right patient
•             Right assessment
•             Right route
•             Right time
•             Right reason
•             Right to refuse medication
•             Right documentation
•             Right patient education
•             Right evaluation

Drug schedules I-V and what does it mean?

Schedule 1- most potential for abuse and dependence, no medicinal qualities

Schedule II- high potential for abuse and dependence, some medicinal qualities

Schedule III- moderate potential for abuse/ dependence, acceptable medicinal qualities, DOCTORS PERSCRIPTION REQUIRED

Schedule IV- low potential for abuse/ dependence, acceptable medicinal qualities, prescription required but fewer filling regulations

Schedule V- lowest potential for abuse/dependence, acceptable medicinal qualities, prescription required- fewest refill regulations
Medical error and what to do if it occurs.

Assess patient, report immediately to prescriber and nurse management, incident report, MAR
Promoting a culture of safety

Patient education- encourage pt to use one pharmacy and not to take RX from another person or previous illness
Pregnancy categories A-D and X- What do they mean?

• Category A: Safest category, no evidence of fetal harm in human studies. 

• Category B: Animal studies show no risk, but human studies are limited. 

• Category C: Potential risk to fetus based on animal studies, but human data is lacking. 

• Category D: Known fetal risk exists, but benefits might outweigh risks in certain situations. 

• Category X: Animal and human studies have shown fetal abnormalities. The drug is contraindicated in women who are or may become pregnant
  Chapter 59 and 60

Review what happens when PSN and SNS are stimulated**
Atropine sulfate/phenylephrine
Glaucoma Patho, types and causes

Inhibition of the normal flow and drainage of aqueous humor, results in increased intraocular pressure

               Angle-closure

               Open- angle

               Causes: unknown

Pilocarpine
Timolol
Review nursing application of eye drops

Look up to the ceiling and place drop in conjunctival sac

Pressure may be applied to the inner canthus for 1-2 minutes to reduce systemic absorption
Otitis media- ear infection of the middle ear

Ear drops how to instill and nursing implications

Adults- pinna up and back

Children younger than 3- pinna down and back
Chapter 15- Unit 2
Types of infection/ super vs opportunistic

Viral, bacterial, fungal, and parasitic

Opportunistic- becomes pathogenic with impaired defense mechanisms

Resistant organisms become predominant strain, causes superinfection
Antibiotic resistance and ways to prevent

Broad spectrum vs Narrow spectrum
Bactericidal vs Bacteriostatic
Chapter 18 URIs and Antibiotics
Penicillin
What happens with beta lactamase?- causes antibacterial activity, inhibits synthesis of bacterial cell walls Why are beta lactamase inhibitors given?- protects PCN from destruction and extended pcns spectrum of efficacy
Amoxicillin and Clavulanate (Augmentin)
Basics about cephalosporins and coverage, contraindications for use, and review patient teaching

Widely used group of medications- Derived from a fungus

Broad-spectrum ATB with activity against gram(+)
and gram(−) bacteria
o More active against gram(−) compared with
PCNs

Widely distributed into most body fluids and tissues-  Maximum concentration in the liver and kidneys

Previous anaphylactic reaction to PCN- Cross-sensitivity low in those with delayed
reactions to PCN, Skin rash, Cephalosporin allergy

Chapter 19- UTIs and antibiotics
Gentamicin
Fluroquinolones/Ciprofloxacin
Chapter 20
Tetracycline hydrochloride
Chapter 21
Erythromycin
Metronidazole
Vancomycin
Chapter 31-Cough- and use of cough medications and when indicated
Pseudonepedrine
Dextromethorphan
Guaifenesin
Chapter 32
Allergic Rhinitis
Diphenhydramine

Final Blue print continued Unit 2 Cardiac- Know then by pharm, class and know MOA of
cardiac meds.
In addition to patient teaching, nursing implications. Use , adverse effects,
contraindications
Blood pressure and how it is regulated

Arterial blood pressure = force exerted on arterial walls by blood flow

Determined by cardiac out (systolic) and peripheral vascular resistance (diastolic)

Autoregulation: ability of body tissues to regulate own blood flow, primarily by nutritional needs of tissues (lack of o2, cellular metabolism by-products)
Effects of elevated BP om body systems

Alters cardiovascular function
Non-pharm measures for htn
Ace inhibitors: Captopril- use in htn and HF
Prazosin
Calcium Channel blocker Amlodipine
Diuretics: HCTZ and Furosemide- Use in HTN and HF
Nitropruside use in HTN Crisis
Beta blockers Metoprolol use in HTn and HF
Digoxin
HF Patho and symptoms of Left vs R side HF

Heart Failure (HF):

• Left-Sided HF Pathophysiology: Ineffective pumping of the left ventricle leads to blood backing up into the lungs (pulmonary congestion).

• Right-Sided HF Pathophysiology: Ineffective pumping of the right ventricle causes blood to back up in the systemic circulation (venous congestion).

Symptoms

Left-Sided HF:

• Pulmonary symptoms: Dyspnea, orthopnea, crackles, pulmonary edema.

• Systemic: Fatigue, tachycardia, decreased urine output.

Right-Sided HF:

• Peripheral symptoms: Edema, jugular vein distension (JVD), hepatomegaly, ascites.

• Systemic: Weight gain, nausea, fatigue.

Review Jeopardy CHF on canvas

Unit 3 Final blueprint
Chapter 41- Diabetes
Difference between Type 1 and Type 2 Diabetes and Risk factors

Type one- autoimmune disorder that destroys pancreatic beta cells, difficult to control

Type two- target cells become unresponsive to insulin due to a defect in insulin receptor function
Signs and Symptoms of hyperglycemia ( polydipsia, polyuria, polyphagia) and hypoglycemia (shaking, sweating, confusion)
DKA Review signs and symptoms
Glyuride
Metformin
For the insulin review Diabetes and CDC pdf on Canvas: onset, peak and duration and type of
insulin and nursing implications
Lispro Humalog
Humulin Regular insulin
Glargine Detemir
Safety administration insulin/nursing implications
GI
Peptic Ulcer disease and risk factors

Ulcers in stomach or duodenum due to mucosal damage (associated with H. pylori)
Constipation- nonpharmacological measures
Omeprazole
Famotidine
Antacids- see powerpoint slide
Sucralfate
Psyllium
Docusate
Ondansetron
Lomotil
Vitamins
Vitamin K
Iron

Unit 4
Parkinson’s Disease- Patho and clinical manifestations
Carbidopa-Levodopa
Benztropine mesylate
Chapter 47
Alzheimer’s Disease- Patho
Memantine
Donepezil
Chapter 53
Seizures Patho
Phenytoin
Phenobarbital
Diazepam

Opioids Nursing Assessment & Interventions

• Assessment: Monitor pain level, respiratory rate, sedation level, BP, and heart rate.

• Interventions: Administer as prescribed, monitor for adverse effects (respiratory depression, constipation), and educate patients on avoiding alcohol.

Opioid Receptors (Mu & Kappa)

• Mu Receptors: Analgesia, euphoria, respiratory depression, physical dependence.

• Kappa Receptors: Analgesia, sedation, dysphoria.

• Adverse Effects: Respiratory depression, constipation, sedation, nausea.

Basic Pathophysiology of Pain

• Pain occurs due to nociceptor activation by tissue damage. Signals are transmitted via the spinal cord to the brain.

Morphine Sulfate

• Use: Severe pain.

• Adverse Effects: Respiratory depression, constipation, sedation.

Naloxone (Narcan)

• Use: Opioid overdose antidote.

• MOA: Competes with opioids at receptor sites.

Inflammation Pathophysiology

• Initiated by tissue injury causing release of inflammatory mediators (histamine, prostaglandins). Increases vascular permeability and recruits immune cells.

Inflammatory Mediators & Pathways

• Include prostaglandins, histamine, cytokines, leukotrienes.

• COX pathway: COX-1 (protective functions), COX-2 (inflammatory).

Acetaminophen (Tylenol)

• MOA: Inhibits COX in the CNS, reducing pain and fever.

• Limitation: Minimal anti-inflammatory effect compared to NSAIDs.

• Adverse Effects: Hepatotoxicity with overdose.

NSAIDs (General)

• MOA: Inhibit COX-1 and COX-2, reducing pain, fever, inflammation.

• Contraindications: GI ulcers, renal impairment, bleeding disorders.

• Adverse Effects: GI bleeding, renal toxicity, cardiovascular risk.

• Patient Teaching: Take with food, avoid concurrent anticoagulants, monitor for bleeding.

Renal Effects of NSAIDs

• Reduce renal blood flow by inhibiting prostaglandin synthesis, causing nephrotoxicity.

Ibuprofen

• Use: Pain, inflammation, fever.

• Adverse Effects: GI bleeding, renal toxicity.

Aspirin

• Use: Pain, fever, anti-platelet.

• Adverse Effects: GI upset, bleeding, tinnitus.

• Reye’s Syndrome: Avoid in children with viral illnesses; causes liver and brain damage.

Gout Pathophysiology

• Uric acid accumulation forms crystals in joints, causing inflammation.

Allopurinol

• Use: Chronic gout.

• MOA: Inhibits xanthine oxidase, reducing uric acid production.

Migraines (Chapter 52)

• Patho: Trigeminal nerve activation, inflammatory neuropeptides, vasodilation.

• Sumatriptan: Selective serotonin receptor agonist; vasoconstricts cranial vessels.

• Adverse Effects: Chest pressure, dizziness.Naproxen

  • Use: Pain, fever, inflammation (e.g., arthritis, menstrual cramps).

  • MOA: NSAID that inhibits COX-1 and COX-2.

  • Adverse Effects: GI irritation/ulcers, renal impairment, cardiovascular risk.

  • Patient Teaching: Take with food; avoid alcohol and other NSAIDs.

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  Chapter 50: Local vs. General Anesthesia

  Local Anesthesia

  • Definition: Numbs a specific area without loss of consciousness.

  • Examples: Lidocaine, bupivacaine.

  • MOA: Blocks sodium channels, preventing nerve impulse transmission.

  General Anesthesia

  • Definition: Causes unconsciousness and lack of sensation for surgical procedures.

  • Examples: Propofol, sevoflurane.

  • Stages: Analgesia, excitement, surgical anesthesia, medullary depression (avoid).

  ---

  Lidocaine

  • Use: Local anesthesia, antiarrhythmic.

  • MOA: Blocks sodium channels, stopping nerve conduction.

  • Adverse Effects: CNS toxicity (tremors, seizures), cardiac arrhythmias if systemic.

  ---

  Chapter 51: General Anesthesia

  Propofol

  • Use: Induction and maintenance of general anesthesia.

  • MOA: Enhances GABA, causing CNS depression.

  • Adverse Effects: Hypotension, bradycardia, respiratory depression.

  • Key Point: Rapid onset and short duration of action.

Chapter 49- 9 questions
Opioids nursing assessment. Interventions when administering them.
Opioid receptors mu and ku review powerpoint when stimulated adverse effects
Basic Patho of pain

Tissue damage activates nociceptors which travels to spinal cord, to thalamus and cerebral cortex
Morphine sulphate

Schedule 2
Naloxone
Chapter 16- 8 questions
Inflammation patho

Inflammatory mediators and pathways- review powerpoint

Localized protective response stimulated by injury to tissues, which serves to destroy, dilute, or wall off (sequester) both the injurious agent and the injured tissue
Acetaminophen MOA and why is it not best to decrease inflammation like the NSAIDS.

it doesn't directly act on inflammatory pathways in the body like NSAIDs do, making it ineffective at reducing inflammation
Know about the drug acetaminophen in general as well
NSAIDS and COX 1 AND COX 2 Review general information on NSAIDS

Contraindications

(COX-1) Supports clotting function of Platelets
 Protects lining of the stomach from acid
 COX-2- Promotes synthesis of prostaglandins
that are involved in inflammatory processes.
adverse effects and patient teaching
NSAIDS and Renal effects

Renal toxicity can occur in patients with
dehydration, heart failure, liver dysfunction, or
use of diuretics or angiotensin-converting
enzyme (ACE) inhibitors.
Ibuprophen
Aspirin
Reye’s syndrome

Acute and potentially life-threatening condition
involving progressive neurologic deficits that can
lead to coma and may also involve liver
damage.
 Triggered by viral illnesses such as influenza as
well as by salicylate therapy itself in the
presence of a viral illness.
 Survivors of this condition may or may not have
permanent neurologic damage
Gout patho

Gout: condition that results from inappropriate
uric acid metabolism
 Underexcretion of uric acid
 Overproduction of uric acid
 Uric acid crystals are deposited in tissues and
joints, resulting in pain
 Hyperuricemia
Allopurinol
Chapter 52- Migraines – 4 questions
Sumatriptan

Naproxen
Chapter 50- 2 questions
Local vs. general anesthesia see powerpoints-
Lidocaine
Chapter 51- General anesthesia- 2 questions
Propafol