Pbd Final Exam Htn

Front 1

How many people in the US are affected with HTN?

Back 1

>65 million

Front 2

What fraction of people over 65 yrs. old have HTN?

Back 2

2/3

Front 3

What percent risk does a normotensive 55 yo person have of developing HTN in their lifetime?

Back 3

90%

Front 4

What percentage of hypertensive patients in the US have their BP controlled?

Back 4

34%

Front 5

What is the primary goal for the Tx of HTN?

Back 5

A reduction in BP and ALSO a reduction in all end-organ damage resulting from HTN

Front 6

How much can a 2 mmHg reduction in SBP reduce stroke mortality?

Back 6

10%

Front 7

What is the target BP for HTN pts with added risk factors such as DM, renal insufficiency, & CAD?

Back 7

130/85

Front 8

What are the perameters of prehypertension?

Back 8

Systolic: 120-139
Diastolic: 80-89

Front 9

What BP is considered hypertensive?

Back 9

140/90

Front 10

What are some risk factors for HTN?

Back 10

Age, obesity, sedentary life style, family Hx, smoking, EtOH, Na+ intake, sex, race

Front 11

How is BP characterized?

Back 11

Variability (changes during the day or at random)
Reactivity (to stress, etc)

Front 12

What is the primary cause of death in benign hypertensive pts?

Back 12

Athersclerotic complications

Front 13

What is the most common form of HTN? What are the symptoms?

Back 13

Chronic benign HTN
Asymptomatic

Front 14

What is the prevalence and prognosis of malignant HTN?

Back 14

Prevalence: 1-5%
Prognosis: 80-90% die within 1 year

Front 15

What are the symptoms of malignant HTN?

Back 15

Headaches
Papilledema (swelling of the optic disc)
Elevated RAAS (renin-angiotensin-aldosterone system)
Hypokalemia

Front 16

Why does hypokalemia result from the RAAS effects of malignant HTN?

Back 16

Aldosterone causes sodium retention but loss of potassium.

Front 17

What is the primary cause of death in malignant hypertensive pts?

Back 17

Target organ damage

Front 18

HTN is a disease of dysregulation of BP. What are the mechanisms that regulate BP? (3) Which is fastest? Which contributes to long-term control?

Back 18

1. Sympathetic NS - fastest
2. Endocrine system
3. Kidney - LT control

Front 19

By what mechanism does the SNS regulate BP?

Back 19

Negative feedback via baroreceptors

Front 20

What are the sub-mechanisms of the endocrine system that regulate BP? (7)

Back 20

Catecholamines
RAAS
ADH (aka vasopressin)
Insulin-hyperinsulinemia-insulin resistance
Local hormones (autocrine/paracrine effects)
ANH
Digitalis-like factor/Natriuretic factor/ouabain-like factor

Front 21

What are the effects of catecholamines on BP?

Back 21

Elevate BP by effecting CO & TPR
(P = CO x TPR)
(CO = HR x SV)

Front 22

What are the effects of RAAS on BP?

Back 22

Effects CO & TPR

Front 23

What are the effects of ADH on BP?

Back 23

Antidiuretic Hormone (AKA vasopressin) effects CO & TPR: fluid retention and vasoconstriction (vasopressin)

Front 24

What are the effects of hyperinsulinemia on BP? (6)

Back 24

1. Antinatriuretic
2. Stimulates SNS to discharge more catecholamines
3. Increases vascular responsiveness
4. Effects transport systems on VSM
5. Insulin resistance causes elevated LDL & reduced HDL
6. Insulin is a growth promotor

Front 25

What are the local hormone factors that affect BP (4) and how?

Back 25

Kinins (vasodilate, diuretic, natriuretic)
PGs (vasodilate, inhibit catecholamine release, natriuretic, diuretic)
EDRF (endothelium derived relaxation factor, with NO - relaxes VSM via cGMP
EDCF (endothelium derived contraction factor - ppotent vasoconstrictor, anti-natriuretic)

Front 26

What are the stimulus & effects of ANH on BP?

Back 26

ANH = atrial natriuretic hormone
Stimulated by increase in atrial pressure (& therefore, an increase in volume)
Volume regulator (increase sodium & water loss; vasodilator)
Decreases aldosterone & ADH (antihypertensive)
Increases GFR by dilating afferent & constricting efferent arterioles
Reduces VSM contractil effects
Decreases renin release
Antagonizes responses to Ang II

Front 27

What are the stimulus & effects of digitalis-like factor on BP?

Back 27

Stimulated by increase in volume
Inhibits Na-K-ATPase
Natriuresis
Increase BP by action at VSM (increase intracellular Na and Ca, reduce NE uptake, enhance vasoconstriction)

Front 28

How does the kidney afffect BP?

Back 28

Pressure diuresis - volume regulation. HTN results when this system fails

Front 29

What % of HTN cases are essential/primary/idiopathic?

Back 29

90-95%

Front 30

What % of HTN cases are secondary?

Back 30

5-10%

Front 31

What are some possible causes of 2ndary HTN?

Back 31

Another disease process - possibly endocrine abnormality, kidney dysfunction, etc

Front 32

T/F There is no current cure for HTN

Back 32

True - treatment is to try to control BP

Front 33

What are the possible causes of primary HTN?

Back 33

Family Hx
Environment (work/stress)
Smoking
EtOH
High salt intake
Age
SNS
Insulin resistance (not DM)
Kidney dysfn

Front 34

What % of the population is genetically susceptible to essential HTN?

Back 34

10-20%

Front 35

What % of HTN pts are salt-sensitive?

Back 35

60%

Front 36

What is the average consumption of NaCl & Na per day in the US, what amount is needed, and what amount is recommended?

Back 36

Consume 9-12 g NaCl (4-5 g Na);
Need ~ 0.5 g Na
Recommended intake 2.4 g Na

Front 37

What % of people with HTN are insulin resistant?

Back 37

50%

Front 38

The losses of what sources of antihypertensive function in the kidney result in essential HTN?

Back 38

Kinins
PGs

Front 39

In the 2 kidney, 1 clip model, what is the initial disturbance, renin response, and LT response?

Back 39

Initial: clipped kidney sees decrerased renal blood flow
Renin response: clipped kidney elevates renin
LT response: other kidney sees increase in volume so does diureses. Renin [c] remaines higher

Front 40

In the 1 kidney, 1 clip model, what is the initial disturbance, renin response, and LT response?

Back 40

Initial disturbance: decreased renal blood flow
Renin response: initially elevated
LT response: Kidney sees more volume, but excess volume, Na, & pressure shut down renin release and renin [c] drops to normal

Front 41

What are the ways the adrenal system cause 2ndary HTN? (4)

Back 41

Pheochromocytoma
Primary Aldosteronism
Secondary Aldosteronism
Cushing Syndrome

Front 42

What is Pheochromocytoma and what are its symptoms in indicating 2ndary HTN?

Back 42

Tumor of the chromaffin cells of the medullary region of adrenal region
Symptomatic triad (in addition to high BP): tachycardia, headaches, attacks of sweating

Front 43

What is the most common cause of 2ndary HTN, and what % of cases does it cause?

Back 43

Primary aldosteronism - 10% of cases

Front 44

What are the effects of primary aldosteronism?

Back 44

Hypokalemia (< 3.0 mEq/L), leading to nephropathy
Low plasma renin tt is not stimulated by low Na diet
Aldosterone not reduced by high Na diet

Front 45

What is Conn's Syndrome and what are the effects of the Captopril test in Conn's patients?

Back 45

Conn's syndrome = autonomous production of aldosterone (primary aldosteronism)
Captopril test = oral captopril (ACE I) will decrease aldo & Ang II in normal pts so ratio of aldo/renin decreases, but this is not the case in Conn's patients, ratio will not decrease

Front 46

What are the effects of Conn's Syndrome on CO and TPR?

Back 46

Both elevated

Front 47

What can cause 2ndary aldosteronism?

Back 47

A functional block of adrenal enzymes to disrupt ACTH feedback, some central ACTH overproduction, or conditions tt elevate renin and/or Ang II

Front 48

How does Cushing's Syndrome lead to 2ndary HTN?

Back 48

Overproduction of adrenal glucocorticoids, which can enhance vascular reactivity to catecholamines (inhibit catecholamine uptake), and increase the synthesis of angiotensinogen & increase number of AT1 receptors. This increases CO by increasing volume (from Na and water retention)

Front 49

What is the prevalence of HTN in pregnancies?

Back 49

10%

Front 50

What is pre-eclampsia and what are the signs?

Back 50

Pre-eclampsia = de nova HTN during late pregnancy
Signs: development of HTN & proteinuria (>300 mg/day) or edema; BP >140/90 after 20th week of gestation.

Front 51

What are some multisystemic problems resulting from pre-eclampsia?

Back 51

Coagulation problems
Liver abnormalities
Epigastric pain
Visual disturbances
Increased perinatal mortality (3x when DBP increases to 95 mmHg)

Front 52

What happens to blood volume in normal pregnancy?

Back 52

Increases 40-60%

Front 53

Why are normal pregnant women not hypertensive?

Back 53

TPR decreases and is hyporesponsive to Ang II although RAS is elevated & BP may even fall

Front 54

What happens to volume, CO, TPR, responsiveness to Ang II, catecholamines, & ADH, and diurnal (daytime) BP rhythms in pre-eclamptics?

Back 54

Volume may not increase
CO is similar to normotensive controls
TPR increases
Responsiveness to Ang II, catecholamines, & ADH is elevated
Diurnal BP rhythms are reversed (reverse circadian rhythms for day & night)

Front 55

What can initiate pre-eclampsia?

Back 55

Hypoperfusion of the placenta

Front 56

What are some other causes of 2ndary HTN besides renal, adrenal, and pre-eclamptic causes?

Back 56

Aortic coarctation
Oral contraceptives
Thyrotoxicosis (increased output of thyroid damage)
Atherosclerosis

Front 57

What are some myocardial complications of HTN? (3)

Back 57

L ventricular hypertrophy (from increased afterload pressure & tissue RAS)
Coronary Artery Disease (CAD; oxygen insufficiency & atherosclerosis)
Congestive heart failure (CHF; depressed cardiac contractility, decreased CO, fluid accumulation)

Front 58

What are some atherosclerotic complications of HTN? (4)

Back 58

Angina
MI
Peripheral Vascular Disease (PVD)
Aneurysm

Front 59

By how much is the risk of athersclerosis changed when systolic BP > 150 mmHg?

Back 59

Risk of atherosclerosis is doubled

Front 60

How does increased BP cause atherosclerosis?

Back 60

- Injury to intima & endothelium
- Sequence of repair leads to atheroma
- Platelet deposition, smooth muscle proliferation
- Complicated with elevated lipids

Front 61

What are some cerebral complications of HTN? (2)

Back 61

Stroke
Transient Ischemic Attack (TIA)

Front 62

How is the risk of stroke affected when SBP > 160 mmHg?

Back 62

Risk of stroke increases 4x

Front 63

What are the common causes of stroke and what are their relative prevalences?

Back 63

Emboli/infarction (10-15%)
Atherothrombosis (70-80%)
Hemorrhage (20-30%)

Front 64

Which organ is the first to be affected by HTN?

Back 64

The eye

Front 65

What does the Keith-Wagener Group describe?

Back 65

Levels of hypertensive retinopathy

Front 66

What are the grades of the Keith-Wagener Group?

Back 66

I - vascular spasm
II - vascular sclerosis
III - homorrhage exudate
IV - papilledema

Front 67

What is the prognosis for pts with Grade I hypertensive retinopathy?

Back 67

81% survival rate

Front 68

What is the prognosis for pts with Grade IV hypertensive retinopathy?

Back 68

7% survival rate

Front 69

What is the prevalence of cardiomegaly in pts with Grade I hypertensive retinopathy?

Back 69

9%

Front 70

What is the prevalence of cardiomegaly in pts with Grade IV hypertensive retinopathy?

Back 70

54%

Front 71

What is the biggest problem with drug Tx for HTN?

Back 71

Patient compliance