Week 8-Lecture 3

Front 1

Tissue effect early on in hypertension is minimal.

Back 1

True

Front 2

Systemic hypertension is

Back 2

Elevated pressures in the systemic arterial bed.

Front 3

What is optimal BP ?

Back 3

S< 120 , D < 80

Front 4

What is normal BP ?

Back 4

<130 , <85

Front 5

When do changes appear at macroscopic and microscopic levels with mild hyperT ?

Back 5

after decades.

Front 6

Where are the primary structural changes in mild hyperT ?

Back 6

blood vessels and heart.

Front 7

Where does wall thickening due to hyaline arteriolosclerosis occur ?(acellular pz material)

Back 7

Arterioles

Front 8

What causes wall thickening in small arteries?

Back 8

Intimal proliferation,elastic reduplication(longstanding hyperT),SM remodelling vs. hypertrophy.

Front 9

What happens to the medium and large arteries in mild hypertension?

Back 9

Atheroma-accelerated.

Front 10

What happens to the heart in mild hyperT ?

Back 10

Coronary atheroma + Concentric LV hypertrophy-(Increased LV mass and thickness > 20 mm)

Front 11

In mild hyperT, kidneys undergo
macroscopically

Back 11

Bilateral atrophy,irrgular scars,granular subscapular surface + reduced cortical thickness( benign nephrosclerosis)

Front 12

During mild hyperT, kidneys undergo microscopically

Back 12

Small cortical infarcts,focal sclerosis in glomeruli,hyaline sclerosis in afferent arterioles

Front 13

In mild hyperT, small arteries in kidneys undergo

Back 13

Intimal proliferation,elastic reduplication,fibrosis,medial hypertrophy.

Front 14

Larger arteries in the kidneys during mild hyperT undergo

Back 14

atheroma.

Front 15

In hypertensive nephrosclerosis,

Back 15

wall of artery is massively thickened.

Front 16

What happens to arterioles in the brain in mild hyperT ?

Back 16

Hyaline sclerosis and Charcot-Bouchard aneurysms(< 1mm) + atheroma in arteries!

Front 17

Name the changes in the basal ganglia and pons with mild hyperT.

Back 17

perivascular spaces,small infarcts and haemorrhages.

Front 18

Retinal circulation is the best microcirculation to observe.

Back 18

True

Front 19

Mild hyperT in the retina produces

Back 19

Focal arteriolar narrowing,exudates(swollen ischaemic retinal neurones), copper wiring and silver wiring(increasing wall thickness with narrowing blood column.) + infarcts 2o to atheroma and variable vessel changes.

Front 20

Atheroma from longstanding hyperT causes

Back 20

Infarcts in the heart,brain,kidneys,guts and limbs.

Front 21

What causes fusiform distal aortic aneurysms?(inherent collagen phenotypes)

Back 21

Atheroma from longstanding hyperT.

Front 22

Name one complication with aortic atheroma.

Back 22

Ulceration with thrombus formation.

Front 23

In the heart,longstanding hypertension leads to

Back 23

1.Cardiac failure with LV hypertrophy which is initially asymptomatic but eventually results in impaired function with progression to failure.
2.Infarction from acc. atherosclerosis.
3. Arrhythmias.

Front 24

Longstanding HT in the brain leads to

Back 24

Intracerebral haemorrhage in white matter of cortex and infarcts assoc. with atheroma and embolic disease.

Front 25

Longstanding HT in kidneys leads to

Back 25

benign nephrosclerosis??-assoc. between BP and risk of end stage renal disease.(major determinant for progression of renal disease of whatever etiology)

Front 26

What can cause limb ischaemia/infarction and gut infarction?

Back 26

Longstanding HT(SMA atheroma for gut)

Front 27

The definition of HT is arbitrary.

Back 27

True.

Front 28

Name the clinical consequences of longstanding HT.

Back 28

Stroke,cerebral h'age,cerebral infarction,CHD-angina,MI & heart failure.Renal failure(5mmHg drop in diast. BP assoc. with 25% fall in risk of end stage renal disease){ many of these problems remain asymptomatic until late in course)

Front 29

What is severe/malignant HT ?

Back 29

When diastolic BP > 110 mmHg and diff. changes are seen in small vessels.Clinical presentation alters.Medical Emergency!

Front 30

What does severe HT do to arterioles?

Back 30

Fibrinoid necrosis-replacement of normal wall by granular eosinophils materials,RBC extravasation,thrombosis,neutrophils in wall.

Front 31

What are the changes in small arteries due to malignant HT ?

Back 31

Florid intimal and medial proliferation-onion skin appearance.

Front 32

What is the no. 1 response in malignant HT ?

Back 32

degeneration and death of walls in arterioles.

Front 33

What happens in proliferative arteriopathy?

Back 33

Cells occluding arteries,no hole in middle and intima has undergone explosive proliferation.(elastic laminae and intimal prolif.)

Front 34

State the change to arterioles in the brain in malignant HT.

Back 34

Fibrinoid necrosis.

Front 35

What happens to neuroglial tissue in malignant HT?

Back 35

oedema and intra-cerebral h'age due to blood-brain barrier breached.

Front 36

Name the pathological changes to arterioles and arteries in case of malignant HT.

Back 36

Fibrinoid necrosis in arterioles and proliferative arteriopathy in small arteries(onion skin)

Front 37

Are glomeruli affected in malignant HT ?

Back 37

Fibrinoid necrosis & fibrinogen,Ig,complement factors in vessel walls.

Front 38

State the changes to the retina in malignant HT.

Back 38

Flame haemorrhage(RBC extrav.),papilloedema and cotton wool spots(ischaemic or infarcted retina)

Front 39

Name the clinical consequences of untreated malignant HT.

Back 39

Brain-encephalopathy,oedema& h'ages.
Kidneys-rapidly progressive renal failure.
Vessels- aneurysms may rupture(weakness in media) ,dissecting aneurysms.

Front 40

What is pulmonary HT ?

Back 40

chronically elevated pulmonary arterial pressures(25 mmHg systole)

Front 41

Name some causes of pulm. HT

Back 41

-2o to lung disease/abnormal lungs.
-congenital cardiac abnormalities(ventr. septal defects)

Front 42

What is anatomical defn. of cor pulmonale?

Back 42

RV hypertrophy due to lung disease.

Front 43

What is the functional defn. of cor pulmonale?

Back 43

RV failure.

Front 44

What happens in cor pulmonale?

Back 44

Diseases of lungs lead to persistent elevation of pulmonary BP and to RV hypertrophy including emphysema,pulm. fibrosis.With time,RV failure.