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Pathophysiology > Partial 3 - Arterial hypertension > Flashcards

Partial 3 - Arterial hypertension Flashcards

1
Q

Normal systolic and diastolic blood pressure

A

Systolic is <120mm Hg

Diastolic is <80mm Hg

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2
Q

Pulse pressure

A

The pulse pressure is the difference between systolic and diastolic pressures and is normally 40, and it may be a better marker of increased CV risks than either of SBP and DBP alone in older persons

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3
Q

The mean arterial pressure can be calculated by

A

Adding 1/3 of systolic pressure to 2/3 of diastolic pressure.

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4
Q

Blood pressure is

A

Cardiac output multiplied by total peripheral resistance

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5
Q

Cardiac output is

A

Stroke volume (amount of blood ejected from the heart with each beat) multiplied with heart rate.

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6
Q

Prehypertensive patients systolic and diastolic pressure

A

Systolic pressure of 120-139 mm Hg

Diastolic of 85-89 mm Hg

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7
Q

Hypertensive stage 1 patients systolic and diastolic pressure

A

Systolic pressure of 140-159 mm Hg

Diastolic pressure of 90-99 mmHg

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8
Q

Hypertensive stage 2 patients systolic and diastolic pressure

A

Systolic pressure of 160 mm Hg or more

Diastolic pressure of 100 mm Hg or more

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9
Q

Hypertension can be decreased by

A 
Weight reduction
Adopting eating plan
Reduction of dietary sodium
Physical activity
Moderation of alcohol consumption.
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10
Q

Which type of hypertension accounts for 90-95% of all cases of hypertension?

A

Primary (Essential) hypertension

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11
Q

Constitutional factors that cause primary hypertension

A

Family history of hypertension (multiple genes are involved, while single genes such as Liddle’s syndrome are uncommon)
Race (blacks are mostly affected)
Age-related hypertension

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12
Q

Lifestyle factors that cause primary hypertension

A

High salt diet
Excessive calorie intake and obesity
Excess alcohol consumption.

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13
Q

Cardiac output and TPR in young hypertensive patients

A

Usually hypertension in young patients there is high resting cardiac output (increased systole) and normal TPR (normal diastole)

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14
Q

Cardiac output and TPR in patients that have had hypertension for 12-20 years

A

In people that have had hypertension in 10-20 years, there is decreased cardiac output, and increased TPR probably due to cardiac and vascular remodelling.

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15
Q

Renin levels in 70% of patients with hypertension

A

Elevated or normal

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16
Q

Changes in TPR may be caused by

A

Altered blood vessel structure
Arterial stiffness
Cell membrane alterations

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17
Q

TPR is controlled by two cell types

A

Vascular endothelial cell

Vascular smooth muscle cell

18
Q

What alteres the blood vessel structure?

A 
Renin angiotensin II
Endothelin
Transforming Growth Factor B1
Insulin like growth factor
Excess response to hemodynamic shear
Decreased nitric oxide
19
Q

Pathogenesis Miscellany

A

Obesity leads to hypertension, and for every ten pounds of weight gain, systolic BP increases by 4.5 mm Hg

Low intake of calcium, potassium and magnesium all is associated with increased BP, and lead also causes hypertension

Use of tobacco increases the BP for 30 minutes after acute ingestion

Caffeine increases BP but one develops tolerance

Even moderate quantities of alcohol may lead to hypertension.

20
Q

Obesity mechanism in hypertension

A 
Increases cardiac output
Increases intravascular volume
Increases RAS (reticular activating system and SNS activity)
Decreases Nitric oxide
Causes hyperinsulinemia
21
Q

Pathogenesis Angiotensin II - Heart

A

Myocardial hypertrophy

Intestinal fibrosis

22
Q

Pathogenesis Angiotensin II - Coronary arteries

A

Endothelial dysfunction with decreased release of nitric oxide
Coronary constriction via release of norepinephrine
Formation of oxygen-derived free radicals via NADH (nicotinamide adenine dinucleotide) oxidase
Promotion of inflammatory response and plaque instability
Promotion of low-density lipoprotein cholesterol uptake

23
Q

Pathogenesis Angiotensin II - Kidneys

A 
Increased intraglomerular pressure
Increased protein leak
Glomerular growth and fibrosis
Increased sodium reabsorption
Decreased renal blood flow
24
Q

Pathogenesis Angiotensin II - Adrenal glands

A

Increased formation of aldosterone

25
Q

Pathogenesis Angiotensin II - Coagulation system

A

Increased fibrinogen

Increased PAI-1 (plasminogen activator inhibitor-1) relative to tissue plasminogen factor

26
Q

Secondary hypertension causes

A 
Renovascular diseases
Renal parenchymal disease
Autosomal dominant polycystic kidney disease
Coarctation of the aorta
Sleep apnea
Pheochromocytoma
Primary aldosteronism (Conn's syndrome)
Cushing syndrome
Hyperparathyroidism
Hypo/hyperthyroidism
Exogenous causes (drugs like cocaine and amphetamines).
27
Q

Postural hypertension

A

It is decrease in standing systolic blood pressure by more than 10 mm Hg, which is usually associated with dizziness/ fainting, and is more frequent in older SBP patients with diabetes, taking diuretics, venodilators, and some psychotropic drugs. BP in these individuals should be monitored in the upright position.

28
Q

Hypertension in women

A

Oral contraceptives may increase BP, and BP should be checked regularly. In contrast, HRT does not raise BP

29
Q

Increased BP may lead to - Heart

A

(1) Increased BP may lead to systolic dysfunction, which leads to decreased ejection fraction, and increased end diastolic volume and left ventricular dilation and thus may result in low cardiac output syndrome
(2) Increased BP may lead to left ventricular hypertrophy which may result in ventricular arrhythmias.
(3) Increased BP may lead to diastolic dysfunction, which leads to normal or increased ejection fraction, normal or decreased end diastolic volume, left ventricular size is normal, which may lead to increased left ventricular filling pressure, and thus results in pulmonary venous congestion and dyspnea

30
Q

Consequences of hypertension - Heart

A 
Chronic Heart Failure (CHF)
LV dysfunction
Myocardial Infarction (MI)
Sudden cardiac death
Ischemic Heart Disease (IHD)
31
Q

Consequences of hypertension - CNS

A

Stroke

Retina damage

32
Q

Consequences of hypertension - Kidneys

A

Renal failure

Proteinuria

33
Q

Does hypertension also lead to peripheral vascular diseases?

A

Yes

34
Q

Liddle’s syndrome (pseudoaldosteronism)

Etiology

A

Autosomal dominat disorder characterized by early and frequently severe hypertension associated with low plasma renin activity, metabolic alkalosis due to hypokalemia and normal to low levels of aldosterone

Etiology:
Dysregulation of an epithelial sodium channel. Increased activity of this channel leads to increased sodium reabsorption, increased extracellular volume and hypertension

35
Q

What treatment in patients with end stage renal failure can increase the blood pressure?

A

Erythropoietin

36
Q

Which parts of the vascular system has the most resistance? (Dr. Najeeb)

A

Arterioles

37
Q

What will arteriolar constriction do to the blood pressure? (Dr. Najeeb)

A

Increase the diastolic blood pressure

38
Q

What is the most potent arteriolar constrictor? (Dr. Najeeb)

A

Angiotensin II

39
Q

Constrictors and Dilators that influence total peripheral resistance (Dr. Najeeb)

A

Constrictors:
Angiotensin II
Cathecolamines
Thromboxane

Dilators:
Nitric Oxide
Prostaglandins
Bradykinin

40
Q

In the presence of epinephrine what will happen to blood vessels with alpha1 and beta2 adrenergic receptors? (Dr. Najeeb)

A

Alpha1 adrenergic : Vasoconstriction

Beta2 adrenergic: Vasodilation

41
Q

Why does oral contraceptive increase risk of hypertension? (Dr. Najeeb)

A

Liver produces more angiotensinogen

42
Q

Function of ANP

A

The main function of ANP is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion

Pathophysiology (20 decks)

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