hypertension for bds 2nd year pathology

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Hypertension - Pathology (BDS 2nd Year)

Based on Robbins & Kumar Basic Pathology and Robbins, Cotran & Kumar Pathologic Basis of Disease

Definition

Hypertension is a sustained elevation of blood pressure. By current criteria, diastolic pressure >80 mm Hg or systolic pressure >120 mm Hg constitutes hypertension. About 40-50% of adults in the general population are affected.

Classification / Types

Type	Frequency	Details
Primary (Essential) Hypertension	90-95% of cases	No identifiable single cause; multifactorial
Secondary Hypertension	5-10%	Due to identifiable cause

Causes of Secondary Hypertension

Renal:

Acute glomerulonephritis
Chronic renal disease
Polycystic kidney disease
Renal artery stenosis
Renin-producing tumors

Endocrine:

Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia
Pheochromocytoma
Acromegaly
Hypothyroidism (myxedema) / Hyperthyroidism
Pregnancy-induced (preeclampsia)
Exogenous hormones (glucocorticoids, oral contraceptives)

Cardiovascular:

Coarctation of the aorta
Polyarteritis nodosa

Neurologic:

Increased intracranial pressure
Obstructive sleep apnea

(Robbins & Kumar Basic Pathology, Table 8.1)

Blood Pressure Regulation (Normal Physiology)

Blood pressure = Cardiac output × Peripheral vascular resistance

Cardiac output is determined by heart rate + stroke volume (which depends on blood volume)
Vascular resistance is regulated at the arteriolar level via neural and hormonal inputs
Kidney is the key regulator through sodium excretion and the RAAS (Renin-Angiotensin-Aldosterone System)

RAAS Pathway:

RAAS diagram - Multiple organs regulate blood pressure. Renin secreted by kidney cleaves angiotensinogen → Angiotensin I → ACE in lung → Angiotensin II → vasoconstriction + aldosterone → Na+ resorption → ↑ blood volume → ↑ BP

Fig: The Renin-Angiotensin-Aldosterone System and its role in blood pressure homeostasis - Robbins, Cotran & Kumar Pathologic Basis of Disease, Fig. 11.4

Pathogenesis of Primary (Essential) Hypertension

Primary hypertension results from complex interplay of genetic and environmental factors that increase blood volume and/or peripheral resistance.

Two Key Mechanisms:

1. Reduced renal sodium excretion:

Reduced Na+ excretion at normal arterial pressure is a key initiating event
This causes obligatory fluid volume expansion → ↑ cardiac output → ↑ BP
The kidney then excretes Na+ at the new higher pressure ("resetting of pressure natriuresis")
A new steady state is achieved but at the expense of elevated BP

2. Increased vascular resistance:

May result from vasoconstriction or structural thickening of vessel walls
Chronic vasoconstriction can cause permanent wall thickening

Genetic Factors:

Familial clustering and twin studies confirm genetic role
Susceptibility genes influence renal sodium resorption, endogenous pressor production, and smooth muscle cell (SMC) growth
Angiotensinogen polymorphisms and angiotensin II receptor variants are implicated in some cases
Single-gene disorders causing rare forms: gene defects in aldosterone metabolism (aldosterone synthase, 11β-hydroxylase, 17α-hydroxylase) → increased aldosterone secretion
Liddle syndrome: mutations in epithelial Na+ channel (ENaC-γ) → exaggerated distal tubular Na+ reabsorption

Environmental Factors:

Stress, obesity, smoking, physical inactivity
High dietary sodium intake - strongest environmental link
Lack of access to healthcare

(Robbins & Kumar Basic Pathology, p. 311)

Morphology (Pathological Changes)

Hypertension causes two main forms of arteriolosclerosis (small vessel disease):

1. Hyaline Arteriolosclerosis

Associated with benign/primary hypertension
Gross/Histology: Thickening of arteriolar walls with deposition of homogeneous, pink hyaline material; loss of underlying structural detail; luminal narrowing
Mechanism: Plasma protein leakage across injured endothelial cells (ECs) into vessel walls + increased extracellular matrix (ECM) production by SMCs in response to chronic hemodynamic stress
Important: Also seen in normotensive elderly individuals and in diabetic microangiopathy (due to hyperglycemia-associated EC dysfunction), but more generalized and severe in hypertension
Kidney effect: Arteriolar narrowing → nephrosclerosis (glomerular scarring)

2. Hyperplastic Arteriolosclerosis ("Onion-Skinning")

Typical of severe/malignant hypertension
Histology: Concentric, laminated thickening of arteriolar walls with luminal narrowing - resembles concentric rings of an onion
The laminations consist of SMCs with thickened, reduplicated basement membrane
In malignant hypertension: accompanied by fibrinoid necrosis (especially prominent in kidneys) - called necrotizing arteriolitis

Histological comparison - (A) Hyaline arteriolosclerosis: thickened arteriolar wall with amorphous pink hyaline deposition, narrowed lumen. (B) Hyperplastic arteriolosclerosis (arrow): concentric "onion-skin" laminated layers causing luminal obliteration (PAS stain)

Fig 8.4: (A) Hyaline arteriolosclerosis - pink homogeneous wall thickening, narrow lumen. (B) Hyperplastic arteriolosclerosis - onion-skin concentric laminations, obliterated lumen (PAS stain) - Robbins & Kumar Basic Pathology

Malignant Hypertension

Approximately 5% of hypertensive patients
Systolic >180 mm Hg or diastolic >120 mm Hg
If untreated: death within 1-2 years
Associated with: renal failure, retinal hemorrhages, papilledema
May arise de novo or be superimposed on pre-existing hypertension
Morphologically: hyperplastic arteriolosclerosis + fibrinoid necrosis

Consequences / Complications of Hypertension

Hypertension is a major risk factor for:

Organ	Consequence
Heart	Ischemic heart disease (IHD), congestive heart failure (most common cause of death - ~50%)
Brain	Stroke (cerebrovascular hemorrhage) - accounts for ~1/3 of deaths
Kidney	Nephrosclerosis (glomerular scarring due to arteriolar narrowing), renal failure
Eyes	Retinal hemorrhages, papilledema (in malignant HTN)
Aorta	Aortic dissection
Vessels	Accelerates atherosclerosis in large and medium arteries

(Robbins & Kumar Basic Pathology, p. 310-312)

Summary Table: Hyaline vs. Hyperplastic Arteriolosclerosis

Feature	Hyaline Arteriolosclerosis	Hyperplastic Arteriolosclerosis
Associated with	Benign/mild hypertension, diabetes, old age	Severe/malignant hypertension
Histology	Homogeneous pink hyaline material	Concentric laminated "onion skin"
Composition	Plasma proteins + SMC-derived ECM	SMCs + reduplicated basement membrane
Lumen	Narrowed	Markedly narrowed/obliterated
Additional lesion in malignant HTN	-	Fibrinoid necrosis (necrotizing arteriolitis)

Key Concepts Summary (Robbins Key Concepts)

Hypertension affects roughly half of adults; major risk factor for atherosclerosis, congestive heart failure, and renal failure
Essential hypertension (90-95%) is multifactorial - involves environmental influences + genetic variants affecting sodium resorption, aldosterone, and the RAAS
Secondary hypertension - caused by single-gene disorders or diseases of kidney, adrenal, or other endocrine organs
Sustained hypertension = increased blood volume + increased peripheral resistance, both from increased renal sodium resorption
Histologically: hyaline arteriolosclerosis (mild HTN) and hyperplastic arteriolosclerosis (severe HTN)

Sources: Robbins & Kumar Basic Pathology (9780323790185), pp. 310-312 | Robbins, Cotran & Kumar Pathologic Basis of Disease (9780443264528), pp. 463-465

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