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Dundee - Autopsy Pathology > 2: Hypertension > Flashcards

2: Hypertension Flashcards

1
Q

Types of hypertension

A

Primary
- unknown cause
- interacting genetic and environmental factors
Secondary
Malignant
- rapidly rising blood pressure leading to death in 1-2 years

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2
Q

Causes of secondary hypertension

A 
○ Renal
			§ Renal artery stenosis
			§ Glomerulonephritis
			§ Chronic renal disease
			§ Renal vasculitis
			§ Polycystic disease
		○ Endocrine
			§ Adrenocorticoid hyperfunction
			§ Exogenous hormones
			§ Phaeochromocytoma
			§ Acromegaly
			§ Hyperthyroidism
		○ Neurologic
			§ Raised ICP
			§ Sleep apnoea
			§ Acute stress
			§ Psychogenic
		○ Cardiovascular
			§ Coarctation of aorta
			§ Polyarteritis nodosa
			§ Increased vascular volume
			§ Increased cardiac output
		○ Pre-eclampsia
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3
Q

What are the main factors influencing blood pressure regulation?

A
  • BP = CO x TPR (Total Peripheral Resistance)
    • CO = SV x HR
    • Renin secreted by the kidneys in response to decreased blood pressure in afferent arterioles
      ○ Renin cleaves angiotensinogen to angiotensin I
      ○ Endothelial catabolism produces angiotensin II
      ○ Regulates blood pressure by increasing vascular SMC tone and increasing adrenal aldosterone secretion
      ○ Increasing renal sodium resorption
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4
Q

Mechanisms of primary hypertension

A

Result of interacting genetic and environmental factors
Blood volume increased by sodium and mineral corticoids
Insufficient renal sodium excretion
Vasoconstrictive influences
Environmental factors

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5
Q

Mechanisms of secondary hypertension

A

○ Renovascular
§ Renal artery stenosis causes decreased glomerular flow and pressure in afferent arteriole of the glomerulus
§ Induces renin secretion leading to increased blood volume and vascular tone via angiotensin and aldosterone pathways
○ Primary hyperaldosteronism
§ Idiopathic
§ Aldosterone-secreting adrenal adenomas
○ Single gene disorders

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6
Q

Morphological features of hypertension

A
  • Hyaline arteriolosclerosis
    ○ Luminal narrowing - intima compressed by media
    ○ Pink hyaline thickening
    • Hyperplastic arteriolosclerosis
      ○ Laminated onion skin thickening of walls - consists of SMCs with thickened reduplicated basement membrane
      ○ Luminal narrowing
      ○ Thickened smooth muscle cells due to basement membrane reduplication
      ○ More likely seen in sever or malignant hypertension
    • Malignant hypertension
      ○ Fibrinoid deposits
      ○ Vessel wall necrosis
      ○ Neutrophil infiltration
      ○ Circumferential bright pink area of necrosis with protein deposition and inflammation
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7
Q

Features of pressure-overload hypertrophy

A 
○ Increased afterload
		○ Causes
			§ Hypertension
			§ Valvular stenosis
		○ New sarcomeres predominantly assemble din parallel to long axes of cells -> concentric increase in wall thickness
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8
Q

Features of volume-overload hypertrophy

A 
○ Increased preload
		○ Causes
			§ Valvular regurgitation
			§ Myocardial infarction
		○ New sarcomeres assembled in series within existing sarcomeres -> ventricular dilation
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9
Q

Features of physiological hypertrophy

A

○ Proportional increase in cell length and width
○ Proportional increase in muscle and lumen size
§ Increased capillary density
○ Normal cardiac function
○ Leads to decreased resting HR and BP
○ Seen in children, pregnancy and athletes
Associated with aerobic exercise

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10
Q

Consequences of hypertrophy

A 
○ Ischaemia-related decompensation -> cardiac failure
		○ Interstitial fibrosis
		○ Arrythmias
		○ Ischaemic heart disease
		○ Sudden cardiac death
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11
Q

Causes of left sided heart failure

A

§ Ischaemic heart disease
§ Hypertension
§ Aortic and mitral valvular disease
§ Primary myocardial disease

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12
Q

Clinical features of left-sided heart failure

A 
○ Symptoms
			§ Dry cough 
			§ Dyspnoea
		○ Signs
			§ 3rd or 4th heart sounds
			§ Tachycardia
			§ Pulmonary oedema - course crackles on auscultation
			§ Atrial fibrillation
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13
Q

Causes of right-sided heart failure

A

Left-sided heart failure

Cor pulmonale

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14
Q

Clinical features of right-sided heart failure

A 
○ Symptoms
Leg swelling
Weight gain
Fatigue
○ Signs
Cyanosis
Distended neck veins
Marked hepatojugular reflex
Ascites
Confusion and irritability
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15
Q

Define cor pulmonale

A

Abnormal enlargement of the right side of the heart as a result of disease of the lungs of pulmonary blood vessels

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16
Q

Causes of cor pulmonale

A 
○ Diseases of pulmonary parenchyma
			§ COPD
			§ Pulmonary fibrosis
			§ Pneumoconiosis
			§ Cystic fibrosis
			§ Bronchiectasis
		○ Diseases of pulmonary vessels
			§ Recurrent PE
			§ Primary pulmonary hypertensin
		○ Disorders affecting chest movement
			§ Kyphoscoliosis
			§ Marked obesity
			§ Neuromuscular diseases
		○ Disorders inducing pulmonary arterial constriction
			§ Metabolic acidosis
			§ Hypoxemia
			§ Chronic altitude sickness
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17
Q

Morphological features of left-sided heart failure

A 
§ Heart 
				□ Depends on disease process
				□ Hypertrophy/dilation of left ventricle
				□ Secondary dilation of left atrium
				□ Nonspecific microscopic changes
			§ Lungs
				□ Heavy wet lungs
				□ Widening of alveolar septa
				□ Haemosiderin-laden macrophages
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18
Q

Morphological features of right-sided heart failure

A 
○ Heart
			§ Depends on cause
			§ Hypertrophy / dilation of right ventricle
		○ Liver and portal systems
			§ Congestive hepatomegaly
			§ Centrilobular necrosis
			§ Cardiac cirrhosis
			§ Congestive splenomegaly
		○ Pleural, pericardia and peritoneal spaces
			§ Effusions
		○ Subcutaneous tissues
			§ Oedema
19
Q

Factors influencing movement of fluid across capillary walls

A 
- Hydrostatic pressure
		○ Blood hydrostatic pressure
		○ Interstitial hydrostatic pressure (negligible-lymphatic system)
	- Oncotic pressure
		○ Blood oncotic pressure
		○ Interstitial oncotic pressure (negligible- few proteins in interstitial fluid so always low) 
	- Permeability of vessel wall
		○ Inflammation
20
Q

Categorisation of oedema

A
  • Exudate = protein rich

- Transudate = protein poor

21
Q

Clinical features of oedema

A 
- Peripheral oedema
		○ Often dependent (affected by gravity)
		○ Common in legs/ankles or sacrum
		○ May be pitting 
		○ Tight and shiny appearance
		○ Potential underlying cardiac/renal disease
		○ Can impair wound healing
	- Angioedema
		○ Occurs on hands, feet, eyes, lips, tongue, airways and genitals
		○ Reaction to allergen, idiopathic or genetic 
		○ Swelling of throat can be fatal
	- Pulmonary oedema
		○ SOB, especially when lying down
		○ Haemoptysis
		○ Often 2-3 times normal weight
		○ Frothy, blood-stained fluid on sections (air, oedema and RBCs)
		○ Consequences
			§ Disrupts gas exchange -> hypoxia
			§ Predisposes to bacterial infection
	- Cerebral oedema
		○ Causes
			§ Trauma
			§ Ischaemic stroke
			§ Tumour obstructing fluid drainage
			§ Infections- encephalitis
			§ Haemorrhage
			§ High altitude
		○ Consequences
			§ Widened gyri
			§ Narrow sulci
			§ Can be life threatening
			§ Herniation
			§ Compression of vascular supply
22
Q

Classification of pulmonary oedema

A
  • Haemodynamic oedema
    ○ Caused by increase in hydrostatic pressure, a decrease in oncotic pressure
    § Increased hydrostatic pressure
    □ Left-sided heart failure
    □ Volume overload
    □ Pulmonary vein obstruction
    § Decreased oncotic pressure
    □ Hypoalbuminemia
    □ Nephrotic syndrome
    □ Liver disease
    □ Protein-losing enteropathy
    ○ Fluid accumulates at base of lung first - where hydrostatic pressure is highest
    • Alveolar wall injury
      ○ Increased capillary permeability due to microvascular injury
      § Direct injury
      □ Infections - bacterial pneumonia
      □ Inhaled gases - high concentrations of oxygen, smoke
      □ Liquid aspiration - gastric contents, near-drowning
      □ Radiation
      □ Lung trauma
      § Indirect injury
      □ SIRS - sepsis, burns
      □ Blood transfusion relation
      □ Drugs and chemicals - chemotherapeutic agents, heroin, cocaine
    • Undetermined origin
      ○ High altitude
      ○ Neurogenic pulmonary oedema - CNS trauma
23
Q

Define nephrosclerosis

A
  • Renal pathology associated with sclerosis of renal arterioles and small arteries
    • Strongly associated with hypertension - both cause and consequence of nephrosclerosis
24
Q

Pathogenesis of nephrosclerosis

A

○ Medial and intimal thickening - response to haemodynamic changes, aging, genetic defects
○ Hyalinisation of arteriolar walls - caused by extravasation of plasma protein through injured endothelium and increased deposition of basement membrane matrix
○ Narrowed lumen
○ Decreased perfusion to renal parenchyma
○ Focal ischaemia
○ Glomerulosclerosis and chronic tubulointerstitial injury
○ Decreased functional renal mass

25
Q

Features of malignant nephrosclerosis

A 
○ SBP> 180mmHg or DBP > 120 mmHg
		○ Endothelial damage
		○ Increases fibrinogen permeability -> fibrinoid necrosis
		○ Increased permeability to proliferative factors -> hyperplastic arteriolosclerosis 
		○ Onion skin intima
		○ Necrotic media infiltrated by fibrin
		○ Narrowed lumen
		○ Reduced renal parenchyma
		○ RAAS activation and increased BP
26
Q

Morphological features of nephrosclerosis

A
  • Gross
    ○ Normal or moderately reduced in size
    ○ Cortical surfaces have fine granularity - due to cortical scarring and shrinking
    • Histologically
      ○ Narrowing of lumens of arterioles and small arteries by hyaline arteriolosclerosis
      ○ Microscopic subcapsular scars with sclerotic glomeruli and tubular dropout
      ○ Interlobular and arcuate arteries show medial hypertrophy, replication of internal elastic lamina and increased myofibroblast tissue in intima
      ○ Consequences of vascular narrowing
      § Foci of tubular atrophy and interstitial fibrosis
      § Variety of glomerular alterations
      □ Collapse of GBM
      □ Deposition of collagen within Bowman space
      □ Periglomerular fibrosis
      □ Total sclerosis of glomeruli
      § Wedge shape infarcts or regional scars
27
Q

Clinical features of nephrosclerosis

A

Features of CKD
§ Stages 1/2 = asymptomatic
§ Stages 3/4 = oedema (Na+ retention), fatigue ( reduced EPO release), pruritis (uraemia), anorexia
§ Stage 5 = oliguria (reduced GFR), ecchymosis (uraemia), confusion (uraemia), insomnia
○ Features of hypertension
§ Stage 1 = no signs of end organ damage
§ Stage 2 = LV hypertrophy, hypertensive retinopathy, atherosclerosis
§ Stage 3 = angina, MI, heart failure, retinal haemorrhages, exudates, papilloedema, stroke, aneurysm, vascular dementia

28
Q

Groups at risk of nephrosclerosis

A 
○ African descent
		○ More severe hypertension
		○ Diabetes mellitus
		○ Older age
		○ Chronic kidney disease
		○ glomerulonephritis
29
Q

How does renal artery stenosis cause hypertension?

A
  • Increased production of renin from ischaemic kidney
    ○ Reduced renal perfusion detected by juxtaglomerular apparatus
    ○ Increased renin converts angiotensinogen to angiotensin I
    ○ ACE converts angiotensin I to angiotensin II
    ○ Aldosterone from adrenal cortex
    § Na+ and H2O retention
    § Increased circulating volume
    ○ Vasoconstriction
    § Increased BP
    ○ Increased perfusion pressure
30
Q

Morphological features of renal artery stenosis

A 
- Commonly caused by atheromatous plaque
		○ Concentrically placed
		○ Superimposed thrombosis
	- Fibromuscular dysplasia
		○ Fibrous or fibromuscular thickening involving intima, media or adventitia
	- Ischaemic kidney
		○ Diffuse ischaemic atrophy
		○ Crowded glomeruli
		○ Atrophic tubules
		○ Interstitial fibrosis
		○ Focal inflammatory infiltrates
31
Q

Clinical features of renal artery stenosis

A

○ Bruit on auscultation of affected kidney
○ Features of CKD
§ Stages 1/2 = asymptomatic
§ Stages 3/4 = oedema (Na+ retention), fatigue ( reduced EPO release), pruritis (uraemia), anorexia
§ Stage 5 = oliguria (reduced GFR), ecchymosis (uraemia), confusion (uraemia), insomnia
○ Features of hypertension
§ Stage 1 = no signs of end organ damage
§ Stage 2 = LV hypertrophy, hypertensive retinopathy, atherosclerosis
§ Stage 3 = angina, MI, heart failure, retinal haemorrhages, exudates, Papilloedema, stroke, aneurysm, vascular dementia

32
Q

At risk groups for renal artery stenosis

A 
○ Atherosclerosis
			§ Most common cause of RAS
			§ Commonly causes renal impairment
			§ > 50 years old
			§ Male > Female
			§ Vascular risk factors
		○ Fibromuscular dysplasia
			§ 2nd most common cause of RAS
			§ Rarely causes renal impairment
			§ 15 -50 year olds
			§ Female > Male
			§ Vascular risk factors
33
Q

What are the causes of Cushing syndrome?

A
  • Too much cortical
    • Majority administration of exogenous glucocorticoids
    • ACTH-dependent
      ○ Pituitary adenoma = Cushing disease
      ○ Ectopic corticotrophin syndrome
    • ACTH-independent
      ○ Adrenal adenoma or carcinoma
34
Q

Features of Cushing syndrome

A
  • Fat pad “buffalo” hump
    • Think arms and legs
    • Thin skin -> bruising/tearing
    • Stretch marks
    • Extra face and body hair
    • Thinning hair
    • Red cheeks
    • Round moon face
35
Q

What are the morphological features of the main lesions of Cushing syndrome?

A
  • Pituitary shows changes regardless of course
    ○ Crooke hyaline change
    § Normal granular basophilic cytoplasm of ACTH producing cells in anterior pituitary becomes homogenous and paler
    § Results of accumulation of intermediate keratin filaments in cytoplasm
    • Adrenals
      ○ Cortical atrophy
      § Exogenous glucocorticoids = bilateral cortical atrophy
      ○ Diffuse hyperplasia
      § ACTH-dependent Cushing syndrome
      § Adrenal cortex diffusely thickened and variably nodular
      § Lipid poor zona reticularis comprising of compact eosinophilic cells surrounded by outer zone of vacuolated lipid rich cells
      ○ Macronodular hyperplasia
      § Adrenals almost entirely replaced by prominent nodules of varying sizes
      § Contain mix of lipid-poor and lipid-rich cells
      § Evidence of microscopic nodularity
      ○ Micronodular hyperplasia
      § 1-3mm darkly pigmented micronodules with atrophic intervening areas
      § Pigment believed to be lipofuscin
      ○ Adenoma or carcinoma
      § Functional adenomas or carcinomas are not morphologically distinct from non-functioning adrenal neoplasms
      § Adenomas
      □ Yellow tumours surrounded by thin o well-developed capsules
      □ Composed of cells that are similar to those in normal zona fasciculata
      § Carcinomas
      □ Larger - 200-300g
      □ Unencapsulated
      □ Anaplastic characteristics of cancer
36
Q

Causes of primary hyperaldosteronism

A

○ Bilateral idiopathic hyperaldosteronism
§ Bilateral nodular hyperplasia of aldosterone-secreting zone glomerulus cells of adrenal glands
§ Most common underlying cause
§ Most are sporadic
§ Older individuals
§ Less severe hypertension
○ Adrenocortical neoplasm
§ Aldosterone-producing adenoma (most common) or rarely adrenocortical carcinoma
§ Conn syndrome
□ Solitary aldosterone-secreting adenoma
□ Mid-adult life
□ F:M = 2:1
□ KCNJ5 mutation - encodes potassium ion channel proteins
○ Familial hyperaldosteronism
§ 5% of cases
§ Gene changes

37
Q

Morphology of primary hyperaldosteronism

A

○ Aldosterone-producing adenomas
§ Solitary small (<2cm) well circumscribed lesions
§ More common on left than right
§ Occur in 30- 40
§ Women more than men
§ Buried within gland
§ Do not produce visible enlargement
§ Bright yellow on cut section
§ Composed of lipid-laden cortical cells that more closely resemble fasciculata cells than glomerulosa cells (normal source of aldosterone)
§ Cells uniform in size and shape
§ Modest nuclear and cellular pleomorphism
§ Spironolactone bodies - found after treatment with antihypertensive spironolactone
○ Bilateral idiopathic hyperaldosteronism
§ Diffuse and focal hyperplasia of cells resembling normal zone glomerulosa
§ Hyperplasia often wedge shaped - extending from peripherally to centre of gland
§ Enlargement subtle

38
Q

Clinical features of primary hyperaldosteronism

A

○ Hypertension
○ Cardiovascular compromise
§ Left ventricular hypertrophy
§ Reduced diastolic volume
○ Increase in prevalence of stroke and MI
○ Hypokalaemia
○ Diagnosed by elevated ratios of plasma aldosterone concentration to plasma renin activity

39
Q

Define phaeochromocytoma

A

Tumour of adrenal medulla

  • comprised of chromaffin cells (neuroendocrine cells)
  • synthesise and secrete catecholamines +/- peptide hormones
  • surgical correctable cause of hypertension
40
Q

Clinical features of phaeochromocytoma

A

○ Of the 90% with HTN, 2/3 have ‘paroxysmal’ episodes of sudden rise in BP, HR & palpitations (can be fatal), headache, sweating, tremor, sense of apprehension
○ Occasionally abdo/chest pain, nausea, vomiting
○ PPT by emotional stress, exercise, change in posture, palpation of tumour
○ Most have chronic, sustained background HTN in addition to paroxysmal symptoms
○ Catecholamine surges can PPT acute CCF, pulmonary oedema, MI, VF and CVA
○ Catecholamine cardiomyopathy: focal necrosis, mononuclear infiltrate, interstitial fibrosis (? Direct effect of catecholamines on myocytes or secondary to vascular constriction-associated ischaemia)

41
Q

Rule of 10s of phaeochromocytoma

A

○ 10% are extra-adrenal (e.g. carotid body)
○ 10% of sporadic cases are bilateral (50% of familial cases)
○ 10% are malignant (i.e. metastasize)
○ 10% are NOT associated with hypertension

42
Q

Familial syndromes associated with phaeochromocytoma

A

○ Due to oncogenic germline mutation affecting a least a dozen genes which fall in to two main classes:
○ Those that enhance growth factor receptor pathway signalling (RET, NF1)
○ Those that increase activity and stability of hypoxia-induced transcription factors (HIF-1α, HIF-2α)
○ Patients present at a younger age than sporadic cases
○ More likely to be bilateral

43
Q

Morphological features of phaeochromocytoma

A
  • Gross
    ○ Weight range: 1g – 4kg (average 100g)
    § Small, intra-adrenal circumscribed lesion
    § Large, haemorrhagic mass, well demarcated by connective tissue or compressed cortical or medullary tissue, necrotic
    § Remnants of adrenal gland stretched over surface
    ○ Cut section
    § Yellow/tan to large, haemorrhagic, necrotic and cystic
    ○ Sites of metastasis
    § Regional LNs, liver, lung, bone
    • Micro
      ○ Nest-like clusters of polygonal/spindle-shaped chromaffin cells surrounded by support cells and rich vascular network.
      ○ Cytoplasmic granules of catecholamines stain with silver stains
      ○ Nuclei round/ovoid with stippled “salt and pepper” chromatin
      ○ Usual signs of aggressive/malignant tumour behaviour (mitoses, necrosis, spindle morphology) unreliable predictors of metastatic potential
44
Q

Provide a brief overview of the different multiple endocrine neoplastic syndromes.

A
  • Group of inherited diseases resulting in proliferative lesions of multiple endocrine organs
    • Distinct features
      ○ Occur at younger age
      ○ Arise in multiple endocrine organs either simultaneously of metachronously
      ○ Tumours multifocal
      ○ Preceded by asymptomatic stage of hyperplasia
      ○ More aggressive and recur at a higher proportion

Dundee - Autopsy Pathology (11 decks)

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