PATHO: MODULE 5

Renal system functions

Maintains homeostasis (fluid balance, electrolytes, acid-base, blood pressure) and removes metabolic waste (urea, creatinine) and toxins via urine

Kidney structure

Cortex (outer, contains glomeruli)

Renal corpuscle

Glomerulus + Bowman’s capsule

Glomerular filtration

High-pressure capillaries filter water, electrolytes, glucose, and waste

Bowman’s capsule

Collects filtrate and funnels it into proximal tubule

Proximal tubule function

Reabsorbs 65–70% of filtrate (water, nutrients, Na+) and secretes H+

Loop of Henle function

Creates hypertonic medulla for urine concentration

Loop of Henle descending limb

Permeable to water only → water exits

Loop of Henle ascending limb

Reabsorbs Na+, K+, Cl− and is impermeable to water

Distal tubule function

Reabsorbs Na+ (aldosterone), excretes K+ and H+, regulates acid-base, forms bicarbonate

Collecting duct function

Responds to ADH to increase water reabsorption

Collecting duct cells

Principal cells (Na+/water reabsorption, K+ excretion)

Urinary flow pathway

Kidneys → ureters → bladder → urethra with unidirectional flow and flushing effect against bacteria

Urine output definitions

Normal ≥30 mL/hr

Renal lab values

Creatinine 0.6–1.2 mg/dL (best GFR indicator)

Creatinine clearance

Blood + 24-hour urine estimate of GFR using MDRD or Cockcroft-Gault equations

Urinalysis components

Visual, chemical, microscopic

Proteinuria and albuminuria

Protein in urine indicates kidney damage

Urine concentration measures

Specific gravity 1.003–1.030 (↓ in overhydration or renal failure)

General kidney dysfunction manifestations

Pain (nephralgia), CVA tenderness, abnormal urine (color, odor, turbidity), hematuria, dysuria, urgency, frequency, oliguria

UTI definition and cause

Infection/inflammation of urinary epithelium from ascending bacteria (most commonly E. coli 80%)

UTI risk factors

Female sex, pregnancy, diabetes (glucose feeds bacteria), urinary obstruction, indwelling catheters (CAUTI), sexual activity, spermicide use, neurogenic bladder

UTI pathogens

Community = E. coli

UTI types

Urethritis (often STI), cystitis (bladder), pyelonephritis (kidney)

UTI clinical features and management

Dysuria, urgency, frequency, hematuria, fever, chills, CVA tenderness

Kidney stone pathophysiology

Supersaturation → precipitation → crystallization → aggregation influenced by pH and temperature

Kidney stone types

Calcium oxalate (75–85%, most common), struvite (10%), uric acid (7%)

Kidney stone risk factors and manifestations

Low fluid intake, hypercalcemia, male, age 20–40, diet

Kidney stone evaluation and treatment

CT, KUB imaging

Urinary obstruction

Blockage from stones, tumors, or strictures

Obstruction complications

Hydronephrosis, hydroureter, UTI risk, postrenal AKI, acute tubular necrosis

Glomerular filtration barrier

Endothelium, basement membrane, podocytes

Glomerular damage effects

Decreased GFR, increased BUN/creatinine, increased permeability → protein loss → hypoalbuminemia → edema

Acute glomerulonephritis pathophysiology

Immune complex deposition (often post–Group A β-hemolytic strep) → inflammation

Acute glomerulonephritis manifestations

Hematuria (smoky urine), proteinuria, edema, hypertension, oliguria, ↑ BUN/Cr

Nephrotic syndrome

Non-inflammatory glomerular damage causing massive proteinuria (>3.5 g/day), hypoalbuminemia, edema, hyperlipidemia, lipiduria (liver ↑ lipoproteins)

Nephritic syndrome

Immune-mediated inflammation causing hematuria (RBC casts), mild proteinuria, decreased GFR, oliguria, hypertension, sodium/water retention

Acute kidney injury (AKI) definition

Sudden, often reversible decline in kidney function causing fluid, electrolyte, and waste imbalance

AKI types

Prerenal (hypoperfusion: hypotension, hypovolemia, hemorrhage, low CO), Intrarenal (kidney damage: ATN, toxins, inflammation), Postrenal (obstruction: stones, tumors, prostate, neurogenic bladder)

AKI pathophysiology

Reduced perfusion ↓ GFR → ischemia → acute tubular necrosis if prolonged (<20% perfusion)

AKI phases

Initiation (rising BUN/Cr), Oliguric (↓ urine, ↑ waste, hyperkalemia, metabolic acidosis), Recovery (diuresis, improving labs)

AKI clinical manifestations

Oliguria/anuria, azotemia (↑ urea/creatinine), uremia, hyperkalemia, metabolic acidosis, hypertension, fluid overload

Uremia

Systemic symptoms from toxin buildup including fatigue, nausea, vomiting, pruritus, neurologic changes

Chronic kidney disease (CKD) definition

Progressive, irreversible nephron loss lasting ≥3 months or GFR <60

CKD causes

Diabetes mellitus and hypertension

CKD stages by GFR

Stage 1 >90

CKD progression

Early: no symptoms

CKD systemic manifestations

Hypertension, cardiovascular disease, anemia, metabolic acidosis, electrolyte imbalance, bone/mineral disorders, malnutrition, depression

CKD anemia

Due to decreased erythropoietin production and uremic toxin effects on RBCs

CKD electrolyte and metabolic changes

Sodium loss, potassium retention (hyperkalemia), metabolic acidosis, hyperphosphatemia, hypocalcemia

CKD bone disease

Caused by phosphate retention and lack of vitamin D activation → secondary hyperparathyroidism → brittle bones

CKD skin findings

Pruritus from urea crystals

CKD cardiovascular risks

Hypertension, heart failure, atherosclerosis, dysrhythmias from electrolyte imbalance

CKD management

Slow progression and manage complications (control BP <130/80, diabetes, electrolytes, anemia with EPO)

Dialysis indications

Stage 5 CKD or severe complications (uremia, refractory hyperkalemia, volume overload)

Hemodialysis

Machine filters toxins and waste when kidneys fail

CKD progression indicator

Declining GFR is most reliable measure

GI tract order

Duodenum → Jejunum → Ileum → Cecum → Appendix → Colon → Sigmoid → Rectum

Small intestine function

Primary site of digestion and absorption of carbohydrates, proteins, fats, vitamins, and minerals

Large intestine function

Absorbs water and electrolytes, forms and stores feces, supports gut microbiota which synthesize vitamins (vitamin K, B vitamins)

Gastric mucous neck cells

Stimulated by irritation/prostaglandins

Parietal cells

Stimulated by ACh, gastrin, histamine

Chief cells

Stimulated by ACh and acid

Enterochromaffin-like cells

Stimulated by ACh and gastrin

G cells

Stimulated by ACh, amino acids, peptides

Common GI dysfunction manifestations

Anorexia, nausea, vomiting, retching, projectile vomiting, GI bleeding, abdominal pain, gas, bloating

Abdominal pain types

Parietal, visceral, referred

GI bleeding classification

Upper (esophagus, stomach, duodenum) vs lower (jejunum, ileum, colon, rectum)

GI bleeding manifestations

Hematemesis (vomiting blood), hematochezia (bright red stool), melena (black tarry stool), occult bleeding (hidden)

Constipation

Small, infrequent, difficult bowel movements

Obstipation

Complete inability to pass stool or gas

Diarrhea

Increased frequency and fluidity of bowel movements

Osmotic diarrhea

Increased luminal particles pull water into intestine via osmosis

Secretory diarrhea

Increased secretion and decreased absorption of fluids/electrolytes

Inflammatory diarrhea

Inflamed intestinal wall impairs absorption (often colon)

Dysphagia

Difficulty swallowing due to muscle or nerve dysfunction

Dysphagia causes (MOON)

Mouth lesions, Obstruction, Esophageal stricture, Neurological disorders (stroke, achalasia, Guillain-Barre)

GERD

Chronic reflux of stomach acid or bile into esophagus due to LES dysfunction

GERD pathophysiology

Weak or relaxed LES allows acid reflux → mucosal damage and inflammation

GERD risk factors (COCCOA QHS)

Chocolate, Obesity, Caffeine, Outlet obstruction, QHS eating (before bed), Hiatal hernia, Smoking

GERD manifestations

Heartburn, dysphagia, regurgitation, chest pain

GERD treatment

Lifestyle modification and proton pump inhibitors

GERD complication

Barrett esophagus (columnar epithelium replaces squamous lining)

Hiatal hernia

Protrusion of stomach through diaphragm into thorax

Hiatal hernia characteristics

Slides with position (in when lying down, out when standing)

Hiatal hernia symptoms

Heartburn, chest pain, dysphagia

Hiatal hernia complications

GERD, esophagitis, regurgitation, possible stomach incarceration (surgical emergency)

Intestinal obstruction

Blockage preventing movement of intestinal contents

Mechanical obstruction

Caused by adhesions, volvulus, intussusception, tumors

Functional obstruction (ileus)

Loss of peristalsis (post-op, opioids, anesthesia)

Small bowel obstruction manifestations

Vomiting, reduced absorption, colicky pain, dehydration, shock

Large bowel obstruction manifestations

Diffuse severe abdominal pain, peritonitis

Obstruction diagnostics

Abdominal X-ray or ultrasound

Obstruction treatment

Decompression, fluid/electrolyte replacement, surgery if unresolved

Severe obstruction complications

Ischemia, infarction, peritonitis, sepsis, shock, organ failure, death

Gastritis

Inflammation of stomach lining (acute or chronic)

Acute gastritis

Superficial erosion of mucosa due to NSAIDs, alcohol, chemicals

Acute gastritis symptoms

Epigastric pain, abdominal discomfort, bleeding

Chronic gastritis

Persistent inflammation often due to H. pylori

Chronic gastritis manifestations

Anorexia, fullness, epigastric pain, nausea/vomiting, hematemesis, melena