L43 – The Pathology of Hypertension Flashcards
(32 cards)
What are the guidelines on hypertension BP ?
Repeated resting levels of:
Systolic >140 mmHg; or
Diastolic >90 mmHg
What is hypertension?
Artificial single dividing line between normotension and hypertension
Why is repeated resting BP measured?
Need repeated levels to avoid over-treatment
JNC-7 prehypertension, Stage 1 and 2 hypertension figures?
Prehypertension = 120-139/80-89
Stage 1= 140-159/90-99
Stage 2= >=160/>=100
What is the formual for BP?
CO x TPR
What are the cardiac and non cardiac factors affecting CO?
- Cardiac factors: (change CO)
Heart rate
Contractility - Non-cardiac factors: (change TPR)
- Blood volume
- Na+ (salt) intake
- Level of mineralcorticoid
What are the two types of hypertension?
Essential hypertension= most common
Secondary hypertension
What is the difference in aetiology of hypertension in old and young patients?
Younger patients: low salt, high renin hypertension
Older patients: high salt, low renin hypertension (i.e.
salt overload)
75% these patients with essential hypertension have what stage hypertension? Renin level?
mild (stage I) hypertension (systolic 140-159; or diastolic 90-99)
Renin level may be low / normal / elevated
What is guyton’s theory on hypertension?
Sodium and renal function to blame
High Na+:
1) uptake by arteriole wall
2) increase norepinephrine release
3) increase vasomotor tone
4) increase CO
All cause increase in TPR
Difference in hypertension in old vs. young? (salt vs renin levels)
Younger patients: low salt, high renin hypertension
Older patients: high salt, low renin hypertension (i.e.
salt overload)
What is Folkow’s proposal on hypertension?
neurogenic
Increased adrenergic drive
How can increased adrenergic drive cause hypertension?
acts on β-adrenergic receptors in heart, vessels and RAAS
1) Increase Heart contractility > CO
2) Stimulate a1 receptor > vessel vasoconstriction > increase TPR
3) Activate RAAS to increase salt retention & blood volume + increase vasoconstriction
25 % with essential hypertension have ____?
moderate / severe / accelerated hypertension
What problem is associated with moderate / severe / accelerated hypertension?
Increased peripheral resistance (mostly in kidney)
What are the three factors that increase TPR?
Neural - alpha/ beta adrenergic
Local: autoregulation, pH, hypoxia
Humoral: Angiotensin, thromboxane, leukotrienes
How does neural factor affect TPR?
Alpha adrenergic = contraction
Beta adrenergic = dilatation
What autoregulation mechanisms are there to manage BP?
RAAS negative feedback
Myogenic: vascular SM contract when stretched
How does hypoxia change TPR?
Local reduction in PAO2: local hypoxic vasoconstriction
Global reduction in PAO2 (e.g. hypoventilation): may lead to generalized pulmonary vasoconstriction
Increase viscosity of blood by erythropoeitin and more RBC (polycythemia)
How do Angiotensin and Thromboxane change TPR?
Angiotensin II = potent vasoconstrictor
Thromboxane A2 = major product of prostaglandin synthase = induces platelet aggregation
Discuss effects of Malignant hypertension on BP?
Extremely high BP > high flow > damage vascular endothelium
> plasma constituents enter vascular wall > fibrinoid necrosis > inflammatory cells trigger paradoxical increase in vasoconstrictor (e.g. renin) > positive feedback and further exacerbates BP
Typical BP for malignant hypertension?
above 180/120
How does Malignant hypertension damage kidneys?
Malignant hypertension causes paradoxical release of renin> very high renin and aldosterone levels > Kidney becomes unresponsive to aldosterone > further increase in BP
How is secondary hypertension different from essential?
Has underlying primary cause that CAN be treated
