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44 Cards in this Set

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Tissue effect early on in hypertension is minimal.
True
Systemic hypertension is
Elevated pressures in the systemic arterial bed.
What is optimal BP ?
S< 120 , D < 80
What is normal BP ?
<130 , <85
When do changes appear at macroscopic and microscopic levels with mild hyperT ?
after decades.
Where are the primary structural changes in mild hyperT ?
blood vessels and heart.
Where does wall thickening due to hyaline arteriolosclerosis occur ?(acellular pz material)
Arterioles
What causes wall thickening in small arteries?
Intimal proliferation,elastic reduplication(longstanding hyperT),SM remodelling vs. hypertrophy.
What happens to the medium and large arteries in mild hypertension?
Atheroma-accelerated.
What happens to the heart in mild hyperT ?
Coronary atheroma + Concentric LV hypertrophy-(Increased LV mass and thickness > 20 mm)
In mild hyperT, kidneys undergo
macroscopically
Bilateral atrophy,irrgular scars,granular subscapular surface + reduced cortical thickness( benign nephrosclerosis)
During mild hyperT, kidneys undergo microscopically
Small cortical infarcts,focal sclerosis in glomeruli,hyaline sclerosis in afferent arterioles
In mild hyperT, small arteries in kidneys undergo
Intimal proliferation,elastic reduplication,fibrosis,medial hypertrophy.
Larger arteries in the kidneys during mild hyperT undergo
atheroma.
In hypertensive nephrosclerosis,
wall of artery is massively thickened.
What happens to arterioles in the brain in mild hyperT ?
Hyaline sclerosis and Charcot-Bouchard aneurysms(< 1mm) + atheroma in arteries!
Name the changes in the basal ganglia and pons with mild hyperT.
perivascular spaces,small infarcts and haemorrhages.
Retinal circulation is the best microcirculation to observe.
True
Mild hyperT in the retina produces
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.
Atheroma from longstanding hyperT causes
Infarcts in the heart,brain,kidneys,guts and limbs.
What causes fusiform distal aortic aneurysms?(inherent collagen phenotypes)
Atheroma from longstanding hyperT.
Name one complication with aortic atheroma.
Ulceration with thrombus formation.
In the heart,longstanding hypertension leads to
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.
Longstanding HT in the brain leads to
Intracerebral haemorrhage in white matter of cortex and infarcts assoc. with atheroma and embolic disease.
Longstanding HT in kidneys leads to
benign nephrosclerosis??-assoc. between BP and risk of end stage renal disease.(major determinant for progression of renal disease of whatever etiology)
What can cause limb ischaemia/infarction and gut infarction?
Longstanding HT(SMA atheroma for gut)
The definition of HT is arbitrary.
True.
Name the clinical consequences of longstanding HT.
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)
What is severe/malignant HT ?
When diastolic BP > 110 mmHg and diff. changes are seen in small vessels.Clinical presentation alters.Medical Emergency!
What does severe HT do to arterioles?
Fibrinoid necrosis-replacement of normal wall by granular eosinophils materials,RBC extravasation,thrombosis,neutrophils in wall.
What are the changes in small arteries due to malignant HT ?
Florid intimal and medial proliferation-onion skin appearance.
What is the no. 1 response in malignant HT ?
degeneration and death of walls in arterioles.
What happens in proliferative arteriopathy?
Cells occluding arteries,no hole in middle and intima has undergone explosive proliferation.(elastic laminae and intimal prolif.)
State the change to arterioles in the brain in malignant HT.
Fibrinoid necrosis.
What happens to neuroglial tissue in malignant HT?
oedema and intra-cerebral h'age due to blood-brain barrier breached.
Name the pathological changes to arterioles and arteries in case of malignant HT.
Fibrinoid necrosis in arterioles and proliferative arteriopathy in small arteries(onion skin)
Are glomeruli affected in malignant HT ?
Fibrinoid necrosis & fibrinogen,Ig,complement factors in vessel walls.
State the changes to the retina in malignant HT.
Flame haemorrhage(RBC extrav.),papilloedema and cotton wool spots(ischaemic or infarcted retina)
Name the clinical consequences of untreated malignant HT.
Brain-encephalopathy,oedema& h'ages.
Kidneys-rapidly progressive renal failure.
Vessels- aneurysms may rupture(weakness in media) ,dissecting aneurysms.
What is pulmonary HT ?
chronically elevated pulmonary arterial pressures(25 mmHg systole)
Name some causes of pulm. HT
-2o to lung disease/abnormal lungs.
-congenital cardiac abnormalities(ventr. septal defects)
What is anatomical defn. of cor pulmonale?
RV hypertrophy due to lung disease.
What is the functional defn. of cor pulmonale?
RV failure.
What happens in cor pulmonale?
Diseases of lungs lead to persistent elevation of pulmonary BP and to RV hypertrophy including emphysema,pulm. fibrosis.With time,RV failure.