Patho II Exam 2

What is the function of the kidneys?

• Filtering waste products (urea → protein metabolism, creatinine → muscle metabolism)

• Fluid balance (release renin when low blood volume, BP; RAAS)

• Electrolyte balance (Maintains serum Na⁺, K⁺, Ca²⁺, phosphate, and

  bicarbonate)

• Acid-base regulation (maintains pH by excreting H+, reabsorbs bicarbonate; kidney fails = metabolic acidosis)

• Produces / activates hormones:

  • Erythropoietin

  • Vitamin D activation

How does Erythropoietin relate to the kidneys?

Produced by cells in kidney → triggered by low oxygen → stimulates bone marrow → increase RBC production

If kidneys fail → ↓ EPO → ↓ RBCs → anemia

How does the kidney activate Vitamin D?

Kidneys activate Vitamin D → Calcitriol (active form) → ↑ Calcium absorption in intestines + maintains bone strength

What labs indicate Kidney failure?

• ↑ BUN

• ↑ Creatinine

• Low GFR

What is the normal GFR value?

~125 mL / min

Low = kidney failure

You can lose >75% of nephrons before symptoms→ why CKD is silent early

What is the normal urine output value?

30 to 60 mL / hr

What is Glomerulopathy?

A broad term of disease affecting the kidneys glomeruli (filter)

Ex. Glomerulonephritis

What is Glomerulonephritis?

Immune-mediated inflammation of glomerulus, impairing the kidneys’ ability to filter waste and fluids effectively

What are symptoms of Glomerulonephritis?

• Hematuria and RBC casts found in urine

• Proteinuria (protein in urine)

• Decrease GFR

• Hypertension (retention of fluid → increase BP)

What is the treatment of Glomerulonephritis?

• Corticosteroids and immunosuppressants (prevent inflammation + damage to glomeruli)

• BP control

• Dietary and fluid restriction

Chronic form → risk of ESRD → dialysis or transplant

What is Nephrotic Syndrome?

Damage to glomerular barrier causing massive protein loss

What is the cascade of Nephrotic Syndrome?

• The filtration barrier is broken down → large proteins escape in urine (albumin)

• Albumin loss in urine → hypoalbuminemia

• Fluid leaks from blood vessels to tissues → edema

• Liver detects low protein levels → release albumin + lipoproteins

What are signs of Nephrotic Syndrome?

• Edema

• Hyperlipidemia (from overproduction of lipoproteins)

• Hypercoagulability → risk of DVT / PE (losing antithrombin III, clotting factor)

• Infection risk (lost antibodies)

What is Acute Kidney Injury (AKI)?

Sudden episodes of kidney failure or damage occuring within hours or days

What are the common types of AKI?

• Prerenal (before the kidneys / before entering the kidneys)

• Intrarenal (within the kidneys)

• Postrenal (after the kidneys)

Prerenal AKI

Decrease blood flow into to the kidneys, caused by:

• Dehydration

• Hemorrhage

• Heart failure

Intrarenal AKI

Direct damage to kidney tissue, commonly caused by acute tubular necrosis or nephrotoxins

Glomerulonephritis also a type

What is acute tubular necrosis (ATN)?

Epithelium cells that line the tubules die from ischemia → kidney damage

What is Oliguric Phase of ATN?

Decrease in urine output → accumulation of K+

K⁺ = 7.8 → can cause fatal arrhythmias

How is Oliguric Phase treated?

Sodium Polystyrene Sulfonate (Kayexalate) → removes potassium through GI tract

Postrenal AKI

Obstruction below the kidneys such as BPH, stones, tumors

What are the priority interventions for AKI?

1. Identify high-risk patients early: Dehydration, sepsis, rhabdomyolysis, contrast dye exposure

2. Maintain fluid volume & cardiac output (Adequate perfusion protects tubular cells)

3. Avoid nephrotoxins (NSAIDs, aminoglycosides, IV contrast — use with caution or avoid)

What is Chronic Kidney Disease (CKD)?

Progressive, irreversible kidney damage staged 1-4; damaged kidneys cannot filter blood properly, causing waste to build up over three or more months

What kills CKD patients?

Cardiovascular disease → fluid overload, heart strain, accumulation of toxins

How can the progression of CKD be slowed?

• Glycemic control (diabetic nephropathy → high blood sugar damages nephrons)

• ACE inhibitors + ARBs (reduce proteinuria and slow nephron loss)

• Control BP (hypertension accelerates CKD progression)

• Reduce CVD risk

What are complications of CKD?

• Anemia (↓ EPO → ↓ RBCs)

• Metabolic Acidosis (can’t excrete H+ or reabsorb bicarbonate) → ↓ pH, ↓ HCO₃⁻

• Drug clearance (dose adjustments required, especially in older adults)

What should you increase in CKD diet?

• Calories → prevent muscle breakdown

• Calcium → bone health

• Vitamin D → the kidneys can’t activate it anymore

What should you restrict in a CKD patient?

• Potassium → body can’t excrete anymore; prevents arrhythmias

• Phosphorus → high phosphorus pulls calcium from bones; prevents bone disease

• Sodium → controls BP + fluid

• Fluids → prevent overload

• Protein → reduces BUN load + accumulation of urea (waste)

What treatment is used for End-Stage Renal Disease (ESRD)?

• Dialysis (hemo or peritoneal)

• Kidney transplant

Hemodialysis

Uses AV fistula or graft and done 3x / week

What are nursing priorities for hemodiaylsis?

• Assess for bruit & thrill (whoosing sound → indicates bloackage)

• No BP or IV on that arm with fistula

What is post-treatment after hemodialysis?

Watch for hypotension, dizziness, and nausea

Peritoneal Dialysis

Uses abdominal lining to filter waste and excess fluid; Fluid removed via osmosis (solution high in glucose → draws fluid out)

What are complications of Peritoneal Dialysis

Peritonitis → redness + swelling of lining of abdomen; will manifest as cloudy dialysate drainage

What medication is given to a patient with a Kidney Transplant?

Lifelong Tacrolimus (Prograf) → monitor for hypertension and renal insufficiency

What are signs of acute rejection of Kidney Transplant?

Fever, jaundice, dark urine

May also see Cirrhosis (liver scarring)

What are diuretics?

Medications that increase sodium excretion; “Water follows sodium”

What indications for using diuretics?

• Edema from heart failure, liver disease/cirrhosis, renal disease

• Acute pulmonary edema

• Hypertension

• Glaucoma (reduces intraocular pressure)

What are the classes of diuretics?

• Thiazide & Thiazide-Like Diuretics

• Loop Diuretics

• Carbonic Anhydrase Inhibitors

• Potassium-Sparing Diuretics

• Osmotic Diuretics

Thiazide Diuretics

Blocks chloride pump in kidney distal convoluted tubule; First line therapy for essential hypertension

Ex. Hydrochlorothiazide, Chlorothiazide, Metolazone

What are side effects of Thiazide Diuretics?

• Hypokalemia (↓ K⁺ → digoxin toxicity if too low)

• Hypercalcemia (↑ Ca²⁺)

• Hyperuricemia (excess uric acid in blood, gout)

• Hyperglycemia

What is the onset, duration, and peak of Thiazide Diuretics?

Oral onset: 2 hr

Peak: 4–6 hr

Duration: 6–12 hr

Loop Diuretics

Powerful diuretic that blocks chloride pump in ascending loop of Henle; drug of choice for acute heart failure and pulmonary edema

Ex. Furosemide/Lasix, Bumetanide, Torsemide, Ethacrynic Acid

What are side effects of Loop Diuretics?

• Hypokalemia (increased digoxin toxicity risk)

• Hypocalcemia, Hypomagnesemia, Hypotension

• Hyperglycemia, Hyperuricemia

• Alkalosis

• Ototoxicity (never IV push rapidly; avoid with aminoglycosides or cisplatin)

What are important nursing interventions when giving Loop Diuretics?

• Administer early in the day to avoid nighttime diuresis

• Monitor weight daily (report gain of 3 lbs/day or 5 lbs/week)

• NSAIDs reduce diuretic effectiveness

• Interstitial pulmonary edema post-hypovolemic shock: Furosemide + Albumin

Carbonic Anhydrase Inhibitors

Block carbonic anhydrase at the proximal tubule → sodium bicarbonate and H⁺ lost in urine; primarily used for Glaucoma, mountain sickness, epilepsy, heart failure, and edema

Ex. Acetazolamide, Methazolamide

How does Carbonic Anhydrase Inhibitors work on Glaucoma?

Reduce intraocular pressure by decreasing aqueous humor production

What are side effects of Carbonic Anhydrase Inhibitors?

• Metabolic acidosis (loss of bicarbonate in urine)

• Hypokalemia

• Neuro Effects:

  • Paresthesia

  • Confusion

  • Drowsiness

What are contraindications for Carbonic Anhydrase Inhibitors?

• High-dose aspirin (additive acidosis)

• Sulfonamide or thiazide allergy (cross-sensitivity)

Potassium-Sparing Diuretic

Prevent body from losing too much potassium (hypokalemia). Used for patients on digoxin, antiarrhythmics, or with arrhythmias; also 1st choice for hyperaldosteronism (cirrhosis, nephrotic syndrome)

Ex. Spironolactone/Aldactone, Eplerenone, Amiloride, Triamterene

What are side effects of Potassium-Sparing Diuretics?

• Hyperkalemia: lethargy, confusion, muscle cramps, fatal arrhythmias.

• Hormonal effects for Spironolactone:

  • gynecomastia (enlarged male breasts), decreased libido, hirsutism (excessive dark hair growth in women), menstrual changes

  • Eplerenone does NOT cause these

What contraindications of Potassium-Sparing Diuretics?

• Avoid K⁺-rich foods if levels elevated

• Do not give with ACE inhibitors ARBs w/o checking K+ levels

• Severe renal disease

• Anuria

What organ are Potassium-Sparing diuretics good for?

Spironolactone and eplerenone improve survival in Heart failure

Osmotic Diuretics

Pulls water into bloodstream → excreted; IV administration only. Used for increased intracranial pressure, acute glaucoma, acute renal failure (prevents oliguric phase), and toxic substance clearance

Ex. Mannitol

What are side effects of Osmotic Diuretics?

Rapid fluid shifts can cause acute heart failure or pulmonary edema

What are contraindications for Osmotic Diuretics?

• Severe renal disease

• Pulmonary congestion

• Heart failure

• Dehydration

• Intracranial bleeding

• NOT used in heart failure or cirrhosis.

What are core nursing actions across all diuretics?

1. Daily weights

• Best indicator of fluid status

2. Monitor labs

• K⁺ (most important)

• BUN/Creatinine

3. Give in morning

• Prevents nocturia

4. Watch for orthostatic hypotension

• Due to volume loss

What is the connection of potassium and diuretics?

• Thiazides, Loop Diuretics: decrease K+

  • monitor K + closely + encourage dietary potassium

• Potassium-Sparing Diuretics: increase K+

  • limit K+ rich foods, avoid K+ supplementation unless directed by provider

• Digoxin + loop/thiazide:

  • increases the risk of digoxin toxicity

  • Level of 2.4 ng/mL → hold dose, notify provider

What is pain?

Unpleasant sensory and emotional experience triggered by actual or potential tissue damage; subjective

What are the 4 steps of pain?

1. Transduction (Where pain STARTS)

2. Transmission (Signal traveling)

3. Perception (Pain becomes “real”)

4. Modulation (Pain control system)

Transduction

Happens at site of injury:

• Tissue is damaged → cells release arachidonic acid + kinins

• Enzyme cyclooxygenase (COX) converts arachidonic acid → prostaglandins

• Prostaglandins sensitize nociceptors → lower pain threshold (even light stimuli can feel painful now)

How do NSAIDs work on transduction?

Block COX → ↓ prostaglandins → stops pain before it even starts

Ex. Ibuprofen

Transmission

Pain signal travels:

• Nerve fibers (A-delta and C fibers) → enter spinal cord (dorsal horn) → travels up the spinothalamic tract → brain (thalamus then cortex)

What is the difference between A-delta fibers and C fibers?

A Delta Fibers:

• Fast (myelinated)

• Sharp, stabbing pain (felt immediately after injury)

• Well localized

• Ex. Needle stick = sharp pain

C Fibers:

• Slow (unmyelinated)

• Dull, aching, burning

• Diffuse (more numerous)

• Ex. Needle stick = lingering soreness

Perception

• The brain recognizes the signal as pain

• Assigns meaning and adds emotional response

• Clinical example: morphine changes how brain perceives pain, though it still exist

Modulation

The brain sends signals to spinal cord (descending pathway) to either inhibit pain or enhance it

What is the Gate Control Theory?

Pain is regulated in the spinal cord (dorsal horn) like a gate, can either be closed or open

What happens when the Gate is closed?

Pain is blocked / lessened from activation of large A fibers through pressure or vibration

Ex, Touch, massage, heat, relaxation, positive emotion

What happens when the Gate is open?

Pain is amplified; Small fiber dominate

Ex. Anxiety, fatigue, fear, focus on pain

What are the different categories of pain?

• Duration:

  • Acute

  • Chronic

• Source:

  • Nociceptive

  • Neuropathic

  • Psychogenic

• Location:

  • Somatic

  • Visceral

  • Referred

What are the types of duration pain?

Acute: Short-term pain from recent injury or illness with clear cause and resolves as healing occurs

Chronic: Pain lasting beyond normal healing (months) and may persist without clear injury

What are the types of source pain?

Nociceptive: caused by actual tissue damage or inflammation

Neuropathic: caused by nerve damage or dysfunction

Psychogenic: pain influenced by psychological factors; brain amplifies pain without clear physical cause, but is real to the patient

What are the types of location pain?

Somatic: Well localized in skin, muscle, bones, joints

Visceral: Hard to localize, internal organs

Referred: Felt somewhere else than the source b/c different organs share the same nerve pathways in the spinal cord

What is an example of Referred pain?

• Heart attack → arm/jaw pain

• Diaphragm irritation → shoulder pain

What are Endogenous opioids?

Our body’s natural painkillers such as endorphins and enkephalins that regulate pain, stress, and reward

How do Endogenous opioids work?

Bind to opioid receptors (Mu (μ) and Kappa (κ) Receptors) on G protein-coupled receptors to reduce pain

What are Opioid Agonists?

Exogenous opioids: External substances introduced to the body to treat severe pain → activate the same receptors but carry a higher risk of addiction

What is the effect of activating Mu (μ) receptor?

• Potent analgesia (pain relief)

• Respiratory depressants (dangerous)

• Euphoria and sedation

• Decreased GI motility → constipation

• Pupil constriction (miosis)

• Physical dependence with prolonged use

What is the effect of activating Kappa (κ) receptors?

• Secondary analgesia (sedation)

• Dysphoria (unpleasant mood — opposite of euphoria)

• Pupil constriction (miosis)

What are the common Opioid Agonist medications?

• Morphine

• Fentanyl

• Hydromorphone (Dilaudid)

• Hydrocodone / Oxycodone

• Methadone

• Tramadol

Morphine

Used for moderate to severe pain, post op, and MI; IV onset is immediate

Baseline opioid everything is compared to

What are risk to assess for using Morphine?

• RR before IV dose → Respiratory depression

• BP → Hypotension (vasodilation)

• Constipation

Fentanyl

Very potent opioid

• Chronic severe pain → patch

• Surgery → IV (fast, potent)

What are risk to assess for using Fentanyl?

• RR VERY closely → Extreme respiratory depression

• Patch location & timing

• Signs of overdose → Patch overdose risk (heat increases absorption!)

  • RR = 8 → emergency

Hydromorphone

Used for:

• Severe pain

• When morphine isn’t enough

What are risk to assess for using Hydromorphone?

• ALWAYS check RR before every IV dose

• Pain level

• Sedation

Hydrocodone / Oxycodone (Perc)

Use for moderate → severe pain (oral use); has high abuse potential

What are risk to assess for using Hydrocodone / Oxycodone?

• Pain relief

• Signs of misuse

• Bowel function → constipation

Methadone

• Chronic severe pain

• Opioid use disorder (withdrawal management)

What are risk to assess for using Methadone?

• Cardiac rhythm (ECG if long-term)

• Sedation over time

• Signs of toxicity

Tramadol

↑ serotonin & norepinephrine, and has a low dependence risk:

• Moderate pain

• When trying to avoid stronger opioids

What are risk to assess for using Tramadol?

• Seizures

• Serotonin syndrome (with antidepressants)

• Less respiratory depression (but still possi

What are common Opioid Adverse Effects?

• Respiratory Depression (most dangerous)

• Sedation & Drowsiness (fall risk due to impaired alertness and coordination)

• Dizziness & Anxiety

• Hallucinations (more common in higher doses or renal impairment)

• Miosis (can indicate toxicity)

• Cough Suppression (concern for post-surgical patients who need to deep breathe and cough)

How does opioid use cause constipation?

• ↓ gut motility

• ↑ water absorption

Not caused from tolerance developing

What nursing actions should be implemented for constipation?

• Fluids

• Fiber

• Stool softener

How does opioid use cause Nausea & Vomiting?

• Stimulate chemoreceptor trigger zone (CTZ) in medulla → N/V (common in initial doses)

• Don’t give in pt with GI obstruction → further motility suppression

What effect does opioid use have Cardiovascular?

Causes Orthostatic hypotension → Instruct patients to rise slowly; fall prevention is a priority

What effect does opioid use have on Genitourinary?

• Urinary retention: Monitor urine output; bladder scan as indicated

• Decreased libido with chronic use

What is tolerance?

Body becomes less sensitive to analgesic effect → higher dose is needed over time

NORMAL physiological adaptation

What is Physical dependence?

When the body adapts physiologically to the presence of opioids → Withdrawal if drug stopped