L43 – The Pathology of Hypertension Flashcards Preview

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Flashcards in L43 – The Pathology of Hypertension Deck (32):
1

What are the guidelines on hypertension BP ?

Repeated resting levels of:
 Systolic >140 mmHg; or
 Diastolic >90 mmHg

2

What is hypertension?

Artificial single dividing line between normotension and hypertension

3

Why is repeated resting BP measured?

Need repeated levels to avoid over-treatment

4

JNC-7 prehypertension, Stage 1 and 2 hypertension figures?

Prehypertension = 120-139/80-89

Stage 1= 140-159/90-99
Stage 2= >=160/>=100

5

What is the formual for BP?

CO x TPR

6

What are the cardiac and non cardiac factors affecting CO?

1. Cardiac factors: (change CO)
 Heart rate
 Contractility

2. Non-cardiac factors: (change TPR)
1. Blood volume
2. Na+ (salt) intake
3. Level of mineralcorticoid

7

What are the two types of hypertension?

Essential hypertension= most common

Secondary hypertension

8

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)

9

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

10

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

11

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)

12

What is Folkow’s proposal on hypertension?

neurogenic

Increased adrenergic drive

13

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

14

25 % with essential hypertension have ____?

moderate / severe / accelerated hypertension

15

What problem is associated with moderate / severe / accelerated hypertension?

Increased peripheral resistance (mostly in kidney)

16

What are the three factors that increase TPR?

Neural - alpha/ beta adrenergic
Local: autoregulation, pH, hypoxia
Humoral: Angiotensin, thromboxane, leukotrienes

17

How does neural factor affect TPR?

 Alpha adrenergic = contraction
 Beta adrenergic = dilatation

18

What autoregulation mechanisms are there to manage BP?

RAAS negative feedback

Myogenic: vascular SM contract when stretched

19

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)

20

How do Angiotensin and Thromboxane change TPR?

 Angiotensin II = potent vasoconstrictor

 Thromboxane A2 = major product of prostaglandin synthase = induces platelet aggregation

21

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

22

Typical BP for malignant hypertension?

above 180/120

23

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

24

How is secondary hypertension different from essential?

Has underlying primary cause that CAN be treated

25

Name 3 causes of secondary hypertension.

Phaeochromocytomas (adrenal medulla tumour)

Adrenal adenomas (adrenal cortex tumour)

Structural renal disease (renal artery stenosis)

26

Explain how phaeochromocytoma increases BP?

tumour causes Over-secretion of adrenaline > increase adrenergic drive ...etc

27

Explain how adrenal adenoma causes BP rise?

Renal gland hyperplasia > hyperactivity > excess renin produced > hyperaldosteronism > excess vasoconstrictor effect and too much Na+ reabsorption

Autoregulated by water reabsorption within certain limits

28

Primary hyperaldosteronism is caused by?

Too much body salt for renin level

29

Too much renin for body salt causes which type of hypertension?

Malignant hypertension

30

What are the 4 sites of pathological changes in hypertension?

Heart
Large vessels
Small vessels
Brain

31

List some pathological changes in hypertension in each of 4 locations with pathological changes.

Heart - Left ventricular hypertrophy

Large vessels - atherosclerosis

Small vessels - Fibrinoid necrosis, hypertrophy, aneurysm, atherosclerosis

Brain- haemorrhage, infarction

32

Name some non- pharmaceutical therapy for hypertension?

Weight loss, decrease sodium intake, decrease alcohol intake, exercise

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