Hypertension - Definition, Causes, Pathology, Clinical Features & Complications

1. Definition

2. Causes / Etiology

A. Primary (Essential) Hypertension - 90-95% of cases

• Genetic predisposition (familial aggregation)
• High dietary sodium intake
• Obesity and insulin resistance / hyperinsulinemia
• Sedentary lifestyle
• Excessive alcohol intake
• Sympathetic nervous system overactivity
• Activation of the renin-angiotensin-aldosterone system (RAAS)
• Abnormal intracellular calcium and sodium handling in vascular smooth muscle cells

B. Secondary Hypertension - 5-10% of cases

3. Pathology / Pathophysiology

Key Pathophysiological Mechanisms:

1. Renin-Angiotensin-Aldosterone System (RAAS) activation
   • Angiotensin II causes potent vasoconstriction and aldosterone release → increased Na+ and water retention → raised CO and TPR.
2. Sympathetic nervous system (SNS) overactivity
   • Increases heart rate, myocardial contractility, and peripheral vasoconstriction.
   • Exaggerated vasopressor responses seen in hypertensive patients.
3. Endothelial dysfunction
   • Reduced nitric oxide (NO) synthesis → impaired vasodilation.
   • Increased endothelin (a potent vasoconstrictor).
   • Reactive oxygen species contribute to vascular inflammation.
4. Abnormal renal sodium handling
   • Impaired natriuresis → volume expansion → elevated CO.
5. Vascular remodeling
   • Vascular smooth muscle hypertrophy → irreversibly elevated TPR.
   • Increased intracellular Ca²+ → increased vascular tone.

Pathological Changes in Tissues:

• Blood vessels: Hyaline arteriolosclerosis (benign hypertension) - thickening of arteriolar walls with homogenous eosinophilic material; Hyperplastic arteriolosclerosis ("onion-skin" lesion) - in malignant hypertension; Fibrinoid necrosis of arterioles in accelerated/malignant hypertension.
• Heart: Concentric left ventricular hypertrophy (LVH) due to chronic increased afterload; diastolic dysfunction; eventually systolic dysfunction.
• Kidney: Nephrosclerosis - hyalinization of glomeruli, tubular atrophy, interstitial fibrosis. In malignant hypertension, necrotizing glomerulitis + fibrinoid necrosis.
• Brain: Microaneurysms (Charcot-Bouchard aneurysms) in small penetrating arteries.

4. Clinical Features

• Headache (typically occipital, worse in the morning) - especially in severe hypertension
• Dizziness / tinnitus
• Epistaxis (nosebleeds)
• Visual disturbances (blurring)
• Palpitations

• Elevated blood pressure on repeated measurements
• Fundoscopy (Keith-Wagener-Barker classification):
  • Grade I: Silver wiring (arteriolar narrowing)
  • Grade II: AV nipping (arteriovenous nicking)
  • Grade III: Flame-shaped hemorrhages, cotton-wool spots (soft exudates)
  • Grade IV: Papilledema (malignant hypertension)
• Loud A2 (aortic component of second heart sound)
• Sustained apex beat (LVH)
• S4 gallop (impaired LV relaxation)
• Renal bruits (if renovascular hypertension)

5. Complications

A. Cardiac Complications

• Left ventricular hypertrophy (LVH) - concentric hypertrophy → diastolic dysfunction
• Coronary artery disease / Angina / MI - accelerated atherosclerosis
• Congestive heart failure - initially diastolic, later systolic
• Aortic dissection - especially with severe/uncontrolled hypertension

B. Cerebrovascular Complications

• Ischemic stroke - thromboembolism from atherosclerotic arteries
• Hemorrhagic stroke - rupture of Charcot-Bouchard microaneurysms
• Hypertensive encephalopathy - breakthrough of cerebral autoregulation
• Vascular dementia - chronic microvascular ischemia

C. Renal Complications

• Nephrosclerosis - gradual loss of renal function
• Proteinuria / microalbuminuria - early marker of hypertensive nephropathy
• Chronic kidney disease (CKD) / End-stage renal disease (ESRD) - hypertension is a major cause
• Malignant hypertension → acute renal failure

D. Ocular Complications (Hypertensive Retinopathy)

• Arteriolar narrowing → hemorrhages, exudates → papilledema (Grade IV)

E. Peripheral Vascular Complications

• Peripheral arterial disease (PAD) - 2.5x increased risk in men, 3.9x in women
• Aortic aneurysm formation

Summary Table of Complications:

• Definition: sustained BP ≥130/80 (ACC/AHA) or ≥140/90 (traditional)
• 90-95% is essential (primary); 5-10% is secondary
• Pathophysiology centers on RAAS activation, SNS overactivity, endothelial dysfunction, and vascular remodeling
• Largely asymptomatic until organ damage - the "silent killer"
• Major complications: stroke, MI, heart failure, CKD, and retinopathy (target organ damage)

Enterobius vermicularis (Pinworm / Threadworm)

1. Definition

• Belongs to phylum Nematoda, class Secernentea
• Over 1 billion people infected worldwide; an estimated 40 million in the United States alone
• Prevalence 20-30% in some age groups/communities
• E. vermicularis is the common species; E. gregorii has been reported in Europe, Africa, and Asia
• Humans are the only known natural host - pets are not reservoirs

2. Etiology (Morphology & Life Cycle)

Morphology:

Life Cycle:

1. Ingestion - Infective eggs are swallowed (fecal-oral route) via contaminated hands, food, bedding, clothing, or airborne eggs
2. Hatching - Eggs hatch in the small intestine, releasing larvae
3. Adult location - Adults establish themselves primarily in the cecum, appendix, and ascending colon
4. Mating - Adult males die soon after copulation
5. Nocturnal migration - Gravid females migrate at night to the perianal region to deposit eggs on perianal skin folds
6. Egg maturation - Eggs become infective within 4-6 hours under optimal conditions
7. Auto-infection cycle - Scratching due to pruritus → eggs under fingernails → hand-to-mouth → re-ingestion
8. Retroinfection - Newly hatched larvae may occasionally migrate back from anal skin into the rectum
9. Incubation period - 2-6 weeks from egg ingestion to gravid female migrating to perianal region
10. Female lifespan - Up to 100 days; eggs remain infective in indoor environment for up to 2 weeks

Transmission Routes:

• Fecal-oral (main route) - contaminated hands, food
• Person-to-person - handling contaminated clothing, bedding
• Autoinfection - scratching perianal area → hand-to-mouth
• Environmental surfaces - curtains, carpeting
• Airborne - inhalation of eggs (minor route)

3. Pathology

• Pinworms do not invade host tissues and live their entire life within the intestinal lumen - this is why they rarely cause serious illness
• No tissue invasion → peripheral eosinophilia is generally NOT seen (and elevated eosinophilia should not be attributed to pinworm)
• No elevated IgE - due to low invasiveness
• The female deposits eggs on the perirectal/perianal mucosa, causing local irritation and intense pruritus
• Scratching causes excoriation of the perianal skin, which can lead to secondary bacterial superinfection
• Adult worms are found in the lumen of the appendix and cecum - visible on histology as cross-sections with characteristic lateral alae (identification feature on H&E stain)
• Appendix involvement: Worms are found in the lumen of the appendix; in some cases associated with signs of acute appendicitis, but also found in histologically normal appendices (incidental finding)
• Aberrant migration - Adult worms occasionally migrate to ectopic sites:
  • Vagina, fallopian tubes, uterus, peritoneal cavity → can cause granulomatous reaction, salpingitis, pelvic peritonitis
  • Urethra → urethritis
• Eosinophilic enterocolitis has been rarely reported
• Eggs remain viable and infective outside the body for extended periods

4. Clinical Features

Symptoms:

Associated Features (disputed causal link):

• Teeth grinding at night (bruxism)
• Enuresis (bedwetting) - should be ruled out in evaluation of enuresis
• Weight loss / poor appetite
• Irritability in children

Complications from Aberrant Migration:

• Vaginitis / vulvovaginitis - common in young girls; worms migrate from perianal area to vagina
• Urethritis
• Salpingitis (fallopian tube inflammation)
• Pelvic peritonitis
• Appendicitis (worms occlude lumen; seen especially in Bailey & Love Surgery)
• Eosinophilic granulomas at ectopic sites

Epidemiological Pattern:

• Primarily affects preschool and school-aged children
• Clusters within families and institutions (schools, daycare)
• Also infects primary caregivers of infected children

5. Diagnosis

6. Treatment

• Treat all household members simultaneously (due to high transmission within families)
• Repeat dose at 2 weeks to eliminate worms acquired after first treatment
• Wash bedding, clothing; trim fingernails; maintain hand hygiene

1. E. vermicularis = most common helminthic infection in children in developed countries
2. Lives in cecum/colon; females migrate nocturnally to perianal skin to lay eggs
3. Eggs become infective in 4-6 hours; remain viable for 2 weeks indoors
4. No tissue invasion → NO eosinophilia, NO elevated IgE
5. Classic symptom = nocturnal perianal pruritus causing sleep disturbance
6. Diagnosis = Scotch tape test (NOT stool examination)
7. Treatment = pyrantel pamoate / mebendazole / albendazole (repeat after 2 weeks; treat entire household)