PEMICU 4

CYNTHIA HUSADA
405160173
HYPERTENSION
HYPERTENSION
= Elevated blood pressure
CLASSIFICATION OF HYPERTENSION (JNC 8)
RISK FACTOR

Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.

HOW IS BLOOD
PRESSURE
REGULATED?
1. The heart, which supplies
the pumping pressure
2. The blood vessel tone,
which largely determines
systemic resistance
3. The kidney, which
regulates intravascular
volume
4. Hormones, which
modulate the functions of
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
the other three systems
 BLOOD
PRESSURE
REFLEX

http://www.cvphysiology.com/Blood
%20Pressure/BP012
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
ESSENTIAL HYPERTENSION
> 90% of hypertensive patients have blood pressures that are elevated for no
readily definable reason

1. Genetics
2. Systemic Abnormalities
3. Insulin Resistance, Obesity, and the Metabolic Syndrome
4. Natural History
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
SECONDARY HYPERTENSION
HOW TO KNOW IF IT’S ESSENTIAL OR
SECONDARY HYPERTENSION
1. Age.
If a patient develops hypertension before age 20 or after age 50 (outside the usual
range of EH), secondary hypertension is more likely.
2. Severity.
Secondary hypertension often causes blood pressure to rise dramatically,
whereas most EH patients usually have mild to moderate hypertension.
3. Onset.
Secondary forms of hypertension often present abruptly in a patient who was
previously normotensive, rather than gradually progressing over years as is the
usual case in EH.
HOW TO KNOW IF IT’S ESSENTIAL OR
SECONDARY HYPERTENSION (2)
4. Associated signs and symptoms.
The process that induces hypertension may give rise to other characteristic
abnormalities, identifi ed by the history and physical examination. For example, a
renal artery bruit (swishing sound caused by turbulent blood flow through a
stenotic artery) may be heard on abdominal examination in a patient with renal
artery stenosis.
5. Family history.
EH patients often have hypertensive first-degree relatives, whereas secondary
hypertension more commonly occurs sporadically.
PATIENT EVALUATION
repeated urinary tract infections may suggest the presence of chronic
pyelonephritis with renal damage as the cause of hypertension.

lifestyle behaviors that may contribute to hypertension, such as excessive alcohol

consumption, and the patient’s medications should be reviewed because certain
drugs may elevate blood pressure.

Laboratory tests commonly performed in the initial evaluation of the hypertensive

patient, including general screening for secondary causes, are (1) urinalysis and
measurement of the serum concentration of creatinine and blood urea nitrogen to
evaluate for renal abnormalities; (2) serum potassium level (abnormally low in
renovascular hypertension or aldosteronism); (3) blood glucose level (elevated in
diabetes, which is strongly associated with hypertension and renal disease); (4)
 1. Exogenous Causes

Several medications can elevate blood pressure.

a. oral contraceptives: increased activity of the renin–angiotensin system.
b. glucocorticoids, cyclosporine (an anti-rejection drug used in patients with
organ transplants),
c. erythropoietin (a hormone that increases bone marrow red blood cell
formation and elevates blood pressure by increasing blood viscosity and
reversing local hypoxic vasodilatation),
d. sympathomimetic drugs (which are common in over-the-counter cold
remedies).
e. Nonsteroidal anti-inflammatory drugs can contribute to hypertension
through dose-related augmentation of sodium and water retention by the
kidneys.
f. Ethanol (chronic excessive consumption) and cocaine: increased
sympathetic nervous system activity.
2. Renal Causes
Renal Parenchymal Disease (increased intravascular volume).
Renovascular Hypertension Stenosis (atherosclerosis and fibromuscular
dysplasia)

3. Mechanical Causes
Coarctation of the Aorta (narrowing of the aorta typically located just distal to the
origin of the left subclavian artery)
4. Endocrine Causes

1. Pheochromocytoma: catecholamine secreting tumors of neuroendocrine

cells (usually in the adrenal medulla)
2. Adrenocortical Hormone Excess
a. Mineralocorticoids: aldosterone, increase blood volume by
stimulating reabsorption of sodium into the circulation by the distal
portions of the nephron
b. Glucocorticoids: cortisol, elevate blood pressure when present in
excess amounts via blood volume expansion and stimulated
synthesis of components of the renin–angiotensin system
3. Thyroid Hormone Abnormalities
a. inducing sodium–potassium ATPases in the heart and vessels
b. increasing blood volume
c. stimulating tissue metabolism and oxygen demand, with secondary
accumulation of metabolites that modulate local vascular tone.
CLINICAL SIGNS AND SYMPTOMS
● asymptomatic (general)
● headache,
● epistaxis (nose bleeds),
● dizziness.
● flushing,
● sweating,
● blurred vision,
COMPLICATIONS
Such organ damage can be
attributed to:
(1) the increased workload of the
heart
(2) arterial damage resulting from
the combined effects of the
elevated pressure itself (weakened
vessel walls) and accelerated
atherosclerosis

Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.

Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
HYPERTENSIVE CRISIS
Medical emergency characterized by a severe elevation of blood pressure.

An acute hemodynamic insult (e.g., acute renal disease) superimposed on a

chronic hypertensive state.

As a result of rapid pathologic changes (fibrinoid necrosis) within the blood

vessels and kidneys, a spiraling increase in blood pressure evolves.
NON-PHARMACOLOGIC TREATMENT
Weight Reduction: Each 10 kg of weight loss is associated with a 5 to 20 mmHg
fall in systolic blood pressure.

Exercise: regular aerobic exercise, such as walking, jogging, or bicycling

Diet: a diet high in fruits, vegetables, and low-fat dairy

Sodium: limit salt intake to 6 g of sodium chloride (2.3 g sodium) per day

Alcohol and Caffeine limitations

Smoking Cessation

Relaxation Therapy
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
JNC 8 Hypertension Guideline Algorithm
Heart Failure
HEART FAILURE
the heart is unable to pump blood forward at a sufficient rate to meet the metabolic
demands of the body (forward failure), or is able to do so only if the cardiac filling
pressures are abnormally high (backward failure), or both.
Leonard S. Lilly. Pathophysiology Of Heart
Disease. 5th Ed.
ETIOLOGY
(1) impairment of ventricular contractility (systolic dysfunction)

(2) increase afterload

(3) impairment of ventricular relaxation and filling (diastolic dysfunction)

Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Leonard S. Lilly.
Pathophysiology
Of Heart
Disease. 5th Ed.
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Leonard S. Lilly. Pathophysiology Of Heart Disease. 5th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
Katzung, B. G., & Trevor, A. J. Basic and clinical pharmacology. 11th Ed.
 Chronic Obstructive Pulmonary Disease

https://www.copdfoundation.org/What-is-COPD/Understanding-COPD/What-is-COPD.aspx
https://www.nhs.uk/conditions/chronic-obstructive-pulmonary-disease-copd/
Chronic Obstructive Pulmonary Disease (COPD) is a term used to describe
progressive lung diseases including emphysema, chronic bronchitis, refractory
(non-reversible) asthma, and some forms of bronchiectasis. This disease is
characterized by increasing breathlessness.

Emphysema: the alveoli break down and become larger.

Chronic bronchitis: an inflammation of the airways (damaged of the cilia).

ETIOLOGY
1. Smoking (main cause)
2. Fumes and dust at work
3. Air pollution
4. Genetics: alpha-1-antitrypsin deficiency
Signs and Symptoms of COPD

● Shortness of breath
● Frequent coughing (with and without sputum or phlegm)
● Increased breathlessness
● Feeling tired, especially when exercising or doing daily activities
● Wheezing
● Frequent chest infections
● Tightness in the chest
TREATMENT

● stopping smoking
● inhalers and medications – to help make breathing easier
● pulmonary rehabilitation – a specialised programme of exercise and
education
● surgery or a lung transplant