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CV Final Material > HTN II: Cowley > Flashcards

HTN II: Cowley Flashcards

1
Q

Blacks are 4.2 times more likely to develop:

A

ESRD (end stage renal disease)

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2
Q

HTN is closely associated with

A

heart disease, stroke and renal disease

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3
Q

For every 20 mmHg systolic or 10 mmHg diastolic increase in BP, there is____ mortality from both ischemic heart disease and stroke

A

2X

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4
Q

Hypertension is the____ leading cause of ESRD. “High normal” BP (130-139 / 85-89 mmHg) is associated with ~ _____greater risk of future development of ESRD

A

2nd

3-fold

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5
Q

Gender and risk: Age-specific associations of ischemic heart disease (IHD) with BP is slightly greater for_____; for vascular mortality as a whole, sex is_____

A

women

of little relevance

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6
Q

______ rises progressively with age and elderly people with hypertension are at greater risk for CV disease

A

Systolic BP

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7
Q

Once diastolic pressures rises to _____ your increase your risk for mortality significantly

A

95-99

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8
Q

Essential hypertension is:

A

polygenic and mutlifactorial

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9
Q

Exogenous causes of HTN:

big ol’ list

A

Oral contraceptives (hepatic synthesis of angiotensinogen resulting in increased to AngII and Aldosterone with Na retention).
• Nonsteroidal anti-inflammatory drugs (COX2 inhibitors).
• Cocaine, ethanol, amphetamines, decongestants (increase sympathetic activity).
• Glucocorticoids (central obesity; Na retention).
• Cyslosporin (anti-rejection drug; Na retention).
• Erythropoietin (hormone that stimulates RBC formation; blood viscosity increased).

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10
Q

90% of HTN is ESSENTIAL and the clinical clues are:

A

age of onset: 20-50
family hx
nromal serum K+, unialysis
unknown cause

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11
Q 
Rare mendelian forms
Essential HTN (genes +envir or complex polygenic disease are \_\_\_\_\_ genetic forms
A

PRIMARY

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12
Q

Renovasulcar, renal parenchymal disease, pheochromocytoma, Cushings and coarctation of aorta are ______ forms of HTN

A

secondary

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13
Q

Hypertnesion has lots of co-morbitities:

A 
Atherosclerosis
• Coronary artery disease
• Myocardial infarction
• Stroke
• Congestive heart failure
• Peripheral vascular disease
• Chronic kidney disease 
• Obesity
• Diabetes
• Metabolic syndrome
• Obstructive sleep apnea
• Cognitive impairment
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14
Q

Why is the kidney an important determinant of BP

A

Cardiovascular system is open to the environment

**Na/H20 in must = Na/H2O out to achieve mass balance

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15
Q

How is mass balance of Na/H2O achieved?

A

increase of Na/H2O–> increase blood volume–> will decrease: SNS/ADH/Renin AngII/aldosterone and increase ANP and prostaglandin’s to increase excretion of Na/H20

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16
Q

What is the pressure-natiruesis and role in regulation of BP

A

we have a negative feedback loop

as MAP increase (from 90 to 120) start to see large increase in Na/H20 excretion

17
Q

What are the three determinants of pressure-natriuesis relationship?

A
  1. Vascular resistance (in the afferent areteriole)
  2. GFR
  3. Tubular reabsorption
18
Q

Relationship between pressure and sodium excretion

determined by a balance of

A

“intrinsic factors” and “extrinsic factors”

19
Q

Physical factors

  • Angiotensin II
  • Prostaglandins
  • Kinins
  • ROS (O2H2O2,NO)
  • 20-Hete
A

All intrinsic factors in BP/ and Na excretion balance

20
Q
  • Angiotensin II
  • CNS Sympathetic
  • Aldosterone
  • Vasopressin
  • Atrial Natriuretic Peptide
  • Endothelin
A

all Extrinsic factors in BP/Na excretion balance

21
Q

Antiotensinogen is secreted by the ____

Angiotensinogen–> Ang I via renin secreated from ____

A

liver

kidney

22
Q 
Ang II binds to AT1 and has what affects on these systems
Adrenal gland
Arterial smooth muscle
SNS
Kidney
Brain
heart
A

adrenal gland: increase aldosterone secreation
arterial smooth: vasocnx
SNS: release of Nepi
Kidney: increase renal tubular Na+ resorption
Brain: stims thirst and vasopressin secreation
Heart: enhances cnx adn ventricular hypertrophy

23
Q

As MAP increases, Ang II levles will____

resulting in _____of Na/H20 excreation

A

increase

increase

24
Q

need for renal perfusion pressure to_____ to achieve
sodium and water balance when angiotensin II
levels are increased
What affect does this have on the pressure-natriuresis slope?

A

rise

reduces the slope of the pressure-natriuresis relationship

25
Q

Ang II was infused into dog, but renal perfusion was controlled at normal level; as a result the dog had severe HTN and retention of Na/H2O with pulmonary edema. Once the controller was stopped, the kidneys saw this huge increase in pressure, urine output increased significantly… This demonstrates that:

A

a rise of renal perfusion pressure was required

to achieve Na+ and H2O balance.

26
Q

When the Ang II infusion was done on dog with left kidney clamped, was there regulation of hypertension?

A

Yes, MAP was still maintained despite only one kidney reading the increase in Na and Ang II

27
Q

What happens to the juxtamedullary glomeruli in NE and Ang II uncontrolled situations?

A

see large increase of damage to the glomeruli

28
Q

An individual gets HTN; their Extracellular fluid volume rises, blood volume rises, arterial pressure rises at day zero, what happens to Total peripheral resistance?
(model based on reduced renal mass)

A

day 0 we get a decrease of TPR… then we get slow rise up to 33% increase of TPR by day 14 from HTN
*in this situation; rise of TPR occurs after the hypertension hasdeveloped and, therefore is secondary to the
hypertension and not the cause of the hypertension

29
Q

Individuals with essential HTN: As they increase in age, _____ contributes less to blood pressure and ______ contributes more

A

CO

TPR

30
Q

Salt sensitivity is associated with ______ In both normotensive and hypertenisve humans aged 25 at beginning of study (30 year study)

A

mortality

people both H + S had worse outcomes

31
Q

In rat models that were designed to mimic salt sensitive HTN, what are some significant findings?

A

low renin form of HTN (seen in African Americans)
proteinuria and glomerosclerosis (filtration decreases)
medullary interstitial fibrosis
early stage renal fail

32
Q

When they did the genetic linkage map of CV function from these salt sensitive and salt resistance rats did they see chromosomal relationships?

A

a little association of HTN links in 1,2,3, 7, 11 and 18

not sure if this is important

33
Q

Dahls salt rats showed 2 phases of HTN development.

Phase I

A

increased Na/l intake in thick ascending limb, we get more generation of free radicals and decreased medullary blood flow
See Na/Cl retention that will act to increase BP with increase SNS and AVP activity
this phase is slow and still reversible

34
Q

Dahls salt rats showed 2 phases of HTN development.

Phase II

A

we start to see a destructive positive feedback loop. renal perfusion pressure is high dt increased BP… this causes T cell infiltration and release of cytokines/ang II/inflammation/ fibrosis/proteinuria/glom sclerosis–> further contributes to low medullary blood flow
this phase is hard to reverse and causes destruction

35
Q 
Consequences of prolonged high Na/Cl diet
Heart:
BV:
Kidneys:
arterial P:
A

Heart:cardia hypertrophy/Diastolic + systolic dsyfnx
Blood vessels: oxidative stress/ endothelial dysnfnx/ fibrosis/ decreased vascular elastiticy
Kidneys: glomerular injury and renal fail
Increased arterial pressure

36
Q

Exploitation of rare extreme outliers in families with

monogenic (Mendelian) mutations – all are

A

kidney related.

All mutations affect renal Na+reabsorption; 8 cause hypertension, 9 cause hypotension.

37
Q

Which chromosomes are the ‘HTN’ ones according to the human genome study?

A

1, 2, 3

17 and 18

38
Q

Results of the gene-centric meta analysis in Europe

A

Analyses confirmed 27 previously reported associations and an 11 additional previously described associations.
• Ten of the genes are predicted to be a target for small molecules and therapeutic intervention or drug response stratification.
***genes are involved.. may be therapeutic targets

39
Q

Now that genes associated with HTN have been identified, what is our next step(s)?

A

Identification of sequence variants does not yield
mechanistic insights or targets for drug development.
• Gene variants discovered in human GWAS studies must
now be understood in the context of molecular networks
and pathways that define this complex disease.
• Mechanisms and pathways whereby GWAS nominated
genes must be illuminated in carefully controlled
experimental animal studies.

CV Final Material (16 decks)

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