3. HYPERTENSION
Definition - Hypertension refers to sustained elevation in
systemic arterial blood pressure.
The elevation may be in either systolic or diastolic pressure, or
in both.
A normal upper limit for an adult is 130–139/85–89 mmHg and
any readings consistently above this are considered as
hypertension.
Normal – 120/80mmHg.
4. Types of hypertension
Primary or essential hypertension (90 %).
Secondary hypertension (10%) where there is an underlying
cause, such as renal diseases or tumour of the adrenal medulla.
Malignant hypertension occurs in the younger age groups with
renal and collagen diseases.
Isolated systolic hypertension mainly occurs when a
combination of factors is seen in the elderly, and is due to
increases in cardiac output, increased peripheral resistance and
renal vascular resistance.
5. ETIOLOGY
Although the cause or causes of primary hypertension is
unknown, several risk factors have been identified for its
development:
obesity
stress
cigarette smoking and alcohol consumption
excessive intake of sodium causing fluid retention
family history.
6. Secondary hypertension results from underlying causes such as:
renal diseases
Cushing’s syndrome
hypo/hyperthyroidism
oral contraceptives
excessive alcohol consumption
coarctation (narrowing) of the aorta.
7.
8. PATHPHYSIOLOGY OF PRIMARY
HYPERTENSION
Primary hypertension results from a combination of genetic and
environmental factors which have an effect on renal and vascular
functions.
One of the possible causes of primary hypertension is a deficiency in
the kidney’s ability to excrete sodium, which increases extracellular
fluid volume and cardiac output, resulting in an increase in blood flow
to the tissues.
The increased blood flow to the tissues results in arteriolar
constriction and an increase in peripheral vascular resistance (PVR)
and blood pressure
10. PATHOPHYSIOLOGY OF SECONDARY
HYPERTENSION
Secondary hypertension is caused by diseases of the organs
resulting in a raised PVR and increased cardiac output.
In most cases, the focus is on kidney diseases or excessive
levels of hormones such as aldosterone and cortisol.
These hormones stimulate the retention of sodium and water,
resulting in increased blood volume and blood pressure.
Once the underlying cause is treated, such as with the removal
of the diseased organ, the blood pressure returns to normal.
11.
12. MALIGNANT HYPERTENSION
This is a rapidly progressive hypertension where the diastolic
pressure is in excess of 120 mmHg which can result in
encephalopathy, cerebral oedema and loss of consciousness.
Malignant hypertension does not indicate that there is cellular injury,
but because it is life-threatening, it is considered as an emergency.
If untreated, cerebral oedema and cerebral dysfunction occur,
leading to death of the individual.
Malignant hypertension can cause a variety of complications, e.g.
papilloedema, cardiac failure, cerebrovascular accident and
retinopathy
13. ISOLATED SYSTOLIC HYPERTENSION
This is caused by an increase in cardiac output or PVR and has a
higher incidence in the elderly.
The rigidity of the vessels is often caused by atherosclerosis.
The ageing process leads to hardening of the arteries, increased PVR
and decreased baroreceptor sensitivity.
In isolated systolic hypertension, the systolic blood pressure is over
140 mmHg and the diastolic pressure is less than 90 mmHg.
It is recognised as an important risk factor for cerebrovascular
accident and cardiac failure, and thus should be treated as a medical
emergency.
15. TREATMENT
Non-pharmacological interventions
Advise the patient to restrict sodium intake
cessation of cigarette smoking and excessive alcohol consumption
reduce their stress levels .
Exercise and maintenance of a healthy weight
Pharmacological interventions
Diuretics are prescribed to reduce fluid load, which leads to reduction
in cardiac output, thus helping to reduce blood pressure.
Medications, e.g. beta-blockers, calcium channel blockers and
angiotensin-converting enzyme (ACE) inhibitors, are indicted for the
treatment of hypertension
16. HEART FAILURE
Heart failure is a chronic, progressive condition in
which the heart muscle is unable to pump enough
blood to meet the body’s needs for blood and oxygen.
Basically, the heart can’t keep up with its workload.
17. ETIOLOGY
Heart failure may be caused by a variety of conditions:
acute MI, where there is a loss of myocardial muscle, which
can lead to poor contraction
hypertension
valvular heart disease
inadequate emptying from the left ventricle due to poor
contraction of the myocardium
anaemia resulting from reduced red blood cells.
18.
19.
20.
21. Left-sided heart failure
In left-sided or left ventricular (LV) heart failure, the left
side of the heart does not pump the blood sufficiently or
work harder to pump the same amount of blood.
There are two types of left-sided heart failure.
Heart failure with reduced ejection fraction (HFrEF),
also called systolic failure: The left ventricle loses its
ability to contract normally. The heart can't pump with
enough force to push enough blood into circulation.
22. Heart failure with preserved ejection fraction
(HFpEF), also called diastolic failure (or diastolic
dysfunction): The left ventricle loses its ability to relax
normally (because the muscle has become stiff). The
heart can't properly fill with blood during the resting
period between each beat.
23. Right-sided heart failure
Right-sided or right ventricular (RV) heart failure usually occurs
as a result of left-sided failure.
When the left ventricle fails, increased fluid pressure is, in effect,
transferred back through the lungs, ultimately damaging the
heart's right side.
When the right side loses pumping power, blood backs up in the
body's veins.
This usually causes swelling or congestion in the legs, ankles and
swelling within the abdomen such as the GI tract and liver
24. Congestive heart failure
Blood flow out of the heart slows, blood returning to the
heart through the veins backs up, causing congestion in the
body's tissues.
Often swelling (edema) results. Most often there's swelling
in the legs and ankles.
Fluid collects in the lungs and interferes with breathing,
causing shortness of breath, especially when a person is
lying down. This is called pulmonary edema and if left
untreated can cause respiratory distress.
25. Pathophysiology
The onset of HF may be acute or chronic. It is often associated
with systolic and diastolic congestion and with myocardial
weakness.
This weakness impairs the ability of the heart to pump efficiently.
In acute HF, there is a sudden decrease in the amount of blood
pumped out from both ventricles, which leads to a reduction in
oxygen supply to the tissues.
However, in chronic HF the progression of the disease is gradual
and in the early stages there may be no symptoms of heart failure.
26. Pathophysiology of right heart failure
RHF is associated with the right ventricle being unable to pump
the blood into the pulmonary artery leading into the lungs.
This leads to an increase in volume of the right ventricle during
the end-diastolic phase, which causes an increase in volume of
the right atria.
This in turn increases the volume of blood and pressure in the
systemic venous system.
There is accumulation of blood in some of the major organs – the
liver, the kidneys and the spleen, resulting in enlargement of
these organs and their eventual destruction.
27. Pathophysiology of left heart failure
LHF results from damage to the left ventricular myocardium.
The contraction of the left ventricle is ineffective and it cannot
pump out all the blood it receives from the left atrium
This results in pooling of blood in the left atrium and raised
pressure in the pulmonary veins, which leads to pulmonary
oedema.
Failure of the left ventricle also results in poor cardiac output. As
the cardiac output decreases, perfusion to the tissues also
diminishes, resulting in poor delivery of oxygen and nutrients to
the tissues
35. ANGINA
Definition - Angina is chest pain that occurs when the heart
muscle does not receive enough oxygenated blood.
It is also described as a crushing pain in the chest.
The term is derived from a Latin word meaning to choke.
The pain can radiate through to the back and shoulder, or down
one or both arms, or into the neck and jaw.
36. TYPES OF ANGINA
There are three types of angina:
1. stable angina
2. unstable angina
3. variant angina.
37. STABLE ANGINA
Stable angina is the most common type and it occurs when
there is a greater demand on the heart than usual.
Stable angina is mainly caused by myocardial ischemia.
The pain usually lasts about 3–5 minutes. If the blood flow is
restored by immediate treatment, no permanent damage results
38. UNSTABLE ANGINA
Unstable angina (also known as crescendo angina) is
characterised by a change in frequency, intensity and duration
of pain.
It is more serious than stable angina and is unpredictable.
It can also occur when the person is at rest and is not relieved
by rest or medication.
Patients who develop unstable angina are at risk of having an
MI
39. VARIANT ANGINA
Variant angina is a rare form of angina.
It is thought to occur as a result of coronary artery vasospasm
resulting in diminished blood flow.
Variant angina is very painful and occurs from midnight to
early morning.
It usually occurs at rest and the same time each day
40.
41. PATHOPHYSIOLOGY
Angina results from a blockage in the coronary arteries, which
reduces blood supply to the affected part of the heart muscle.
At rest the blood supply may be sufficient to provide nutrients
and oxygen to the heart muscle; however, during activity, e.g.
walking or running, the heart rate increases which puts more
effort on the heart.
During exertion, if the blood flow to the heart muscle is
inadequate, the oxygen supply is also diminished, leading to
severe pain
45. Myocardial infarction
Myocardial infarction (MI) is commonly referred to as
a ’heart attack’, which results from oxygen starvation
of the myocardium.
When the coronary blood flow is occluded as a result
of a blood clot or fatty deposits (atheromatous plaque)
over a period of time, death of the myocardium will
take place, resulting in MI
46. ETIOLOGY
Abnormal lipid profile
Diabetes mellitus
Psychosocial factors such as depression, loss of
control, global stress, financial stress, and life events
including marital separation, job loss, and family
conflicts
Lack of physical activity
47.
48. PATHOPHYSIOLOGY
An occluded coronary artery results in myocardial
ischaemia due to a lack of oxygen to the myocardial cells.
If the heart tissue is deprived of oxygen for a prolonged
period of time, approximately 20–45 minutes, this can lead
to cell death (necrosis) distal to the occlusion.
Damaged heart tissue conducts electrical signals much
more slowly than normal heart tissue, which can result in
inefficient contraction of the myocardium.
49. This can result in decrease:
volume of blood ejected by the left ventricle with each
heartbeat
cardiac output (volume of blood pumped out by the
left ventricle each minute)
blood pressure
tissue perfusion.
50.
51.
52. Evaluation
The three components in the evaluation of the MI are
clinical features,
ECG findings, and
cardiac biomarkers
54. TREATMENT
Non Pharmacological
Counseling and education of patients
Smoking cessation and avoid alcohol intake
Dietary control (low cholesterol)
Exercise
Weight reduction
55.
56. ATHEROSCLEROSIS/ARTERIOSCLEROSIS
Arteriosclerosis is the term describing arterial disorders in
which degenerative changes result in decreased blood flow.
Atherosclerosis is the most common form of
arteriosclerosis where there is thickening and hardening of
the vessel walls due to lipid accumulation.
This condition is found mainly in the large- and medium-
sized arteries, such as the aorta and its branches, the
coronary arteries and the arteries that supply the brain,
whereas arteriosclerosis mainly affects arterioles
57. ETIOLOGY
The cause of atherosclerosis is not known, but certain risk factors have been
identified:
Hypertension
cigarette smoking (nicotine has a vasoconstricting eff ect)
high lipid levels in the blood
familial history
obesity
diabetes mellitus (high serum glucose levels cause vascular damage)
lifestyle
alcohol
gender (men are at a higher risk than women).
58.
59. PATHOPHYSIOLOGY
Atherosclerosis is a form of arteriosclerosis where the walls
of the arteries are hard, thick and narrow as a result of lipid
accumulation within the arterial walls.
Lipids (low-density lipoproteins [LDL]) are deposited on
the tunica intima of the damaged blood vessel where
oxidation of LDL takes place.
The oxidised LDL then enters the tunica intima of the
arterial wall, where they are ingested by macrophages.
The lipid-filled macrophages then become foam cells.
60. Once the foam cells accumulate in significant numbers, they form
a lesion called a fatty streak, which over time causes a bulge in the
lumen of the blood vessel and this restricts blood flow.
Affected blood vessels become hard, lose their elasticity, restrict
blood flow and eventually occlude the artery.
Greater blood pressure is needed to push the blood through these
narrow blood vessels, which leads to hypertension.
Although atherosclerosis can affect any organ or tissue, the
arteries supplying the heart, brain, small intestines, kidneys and
lower extremities are mostly affected.
61.
62.
63.
64.
65. BRONCHIAL ASTHMA
Asthma is a disease of airways that is characterised by
increased responsiveness of the tracheobronchial tree to a
variety of stimuli resulting in widespread spasmodic narrowing
of the air passages which may be relieved spontaneously or by
therapy.
Asthma is an episodic disease manifested clinically by
paroxysms of dyspnoea, cough and wheezing.
Asthma is a chronic inflammatory disorder of the lungs
66.
67.
68.
69.
70. ETIOPATHOGENESIS AND TYPES
Two broad etiologic types are traditionally described:
extrinsic (allergic, atopic) asthma and
intrinsic (idiosyncratic, non-atopic) asthma
71. 1. EXTRINSIC (ATOPIC, ALLERGIC)
ASTHMA
In extrinsic asthma, airway inflammation is a consequence of
hypersensitive reactions associated with allergy, i.e. pollen, dust mites
or foodstuffs
It usually begins in childhood or in early adult life.
Most patients of this type of asthma have personal and/or family
history of preceding allergic diseases such as rhinitis, urticaria or
infantile eczema.
Hyper sensitivity to various extrinsic antigenic substances or
‘allergens’ is usually present in these cases.
72. Most of these allergens cause ill effects by inhalation e.g.
house dust, pollens, animal danders, moulds etc.
Occupational asthma stimulated by fumes, gases and organic
and chemical dusts is a variant of extrinsic asthma.
There is increased level of IgE in the serum and positive skin
test with the specific off ending inhaled antigen representing
an IgE-mediated type I hypersensitivity reaction which
includes an ‘acute immediate response’ and a ‘late phase
reaction’
73. Acute immediate response is initiated by IgE-sensitised mast
cells (tissue counterparts of circulating basophils) on the
mucosal surface.
Mast cells on degranulation release mediators like histamine,
leukotrienes, prostaglandins, platelet activating factor and
chemotactic factors for eosinophils and neutrophils.
The net effects of these mediators are bronchoconstriction,
oedema, mucus hypersecretion and accumulation of eosinophils
and neutrophils
74. Late phase reaction follows the acute immediate response and
is responsible for the prolonged manifestations of asthma.
It is caused by excessive mobilisation of blood leucocytes that
include basophils besides eosinophils and neutrophils.
These result in further release of mediators which accentuate
the above-mentioned effects.
75. 2. Intrinsic (idiosyncratic, non-atopic) asthma
Intrinsic asthma is linked to hyper-responsive reactions to other forms
of stimuli, e.g. infection, sudden exposure to cold, exercise, stress or
cigarette smoke
This type of asthma develops later in adult life with negative personal
or family history of allergy, negative skin test and normal serum levels
of IgE.
Most of these patients develop typical symptom complex after an
upper respiratory tract infection by viruses.
Associated nasal polypi and chronic bronchitis are commonly present.
There are no recognisable allergens but about 10% of patients become
hypersensitive to drugs, most notably to small doses of aspirin
(aspirin-sensitive asthma).
76. Pathophysiology
The bronchi and bronchioles contain smooth muscle and are lined
with mucous-secreting glands and ciliated cells.
Close to the airway’s blood supply, there are large quantities of mast
cells.
Once stimulated, mast cells release a number of cytokines (chemical
messengers), which cause physiological changes to the lining of the
bronchi and bronchioles.
Three such cytokines are histamine, kinins and prostaglandins, which
cause smooth muscle contraction, increased mucus production and
increased capillary permeability.
77. The airways soon narrow and become flooded with mucus and
fluid leaking from blood vessels
As the airways become obstructed, the patient finds it
increasingly hard to breathe and to cough up the mucus.
If unresolved, fatigue can occur and the patient’s respiratory
effort becomes weak and inadequate, causing hypoxaemia and
in severe cases, hypercapnia.
83. COPD
Chronic Obstructive Pulmonary Disease (COPD)
Chronic obstructive pulmonary disease (COPD) is a
chronic inflammatory lung disease that causes
obstructed airflow from the lungs.
Symptoms include breathing difficulty, cough, mucus
(sputum) production and wheezing.
Obstructive bronchiolitis is a condition in which chronic
inflammation and swelling cause the inside of the breathing
tubes (airways) to be smaller than normal.
84.
85. Chronic bronchitis
Chronic bronchitis irritates your bronchial tubes, which
carry air to and from your lungs. In response, the tubes
swell and mucus (phlegm or “snot”) builds up along the
lining.
The buildup narrows the tube’s opening, making it hard to
get air into and out of your lungs.
86. EMPHYSEMA
This results from damage to your lungs’ air sacs
(alveoli) that destroys the walls inside them and
causes them to merge into one giant air sac. It can’t
absorb oxygen as well, so you get less oxygen in your
blood. Damaged alveoli can make your lungs stretch
out and lose their springiness. Air gets trapped in your
lungs and you can’t breathe it out, so you feel short of
breath.
87.
88.
89.
90.
91.
92.
93.
94.
95.
96. ACUTE RENAL FAILURE
DEFINITION - Acute kidney injury (AKI), previously
known as acute renal failure (ARF), is a condition in
which the kidneys are unable to remove accumulated
metabolites from the blood, leading to altered fluid,
electrolyte and acid–base balance.
i.e acute fall in GFR, thus decreasing the clearance of
metabolic waste products.
97. TYPES
1.Prerenal
Prerenal causes include insufficient blood flow to the
kidneys, resulting in reduced cardiac output as a result of
heart failure, hypovolemia resulting from haemorrhage and
shock.
The kidneys receive 20–25% of cardiac output to maintain
glomerular filtration.
With a reduction in renal blood flow, glomerular filtration
is affected and this causes ischaemic changes to the renal
tissues.
98. 2. Intrarenal
Intrarenal failure results from conditions that impair renal
function.
The renal parenchyma and nephrons are damaged, leading
to renal failure.
Glomerulonephritis, hypertension, chemicals such as ethyl
glycol and drugs, e.g. antibiotics, can all affect renal
function.
The nephrons of the kidneys are susceptible to trauma from
poor renal blood flow, hypertension and shock.
99. The cell membranes of the nephrons are damaged as a
result of the trauma.
The renal tubules become blocked with debris, thus
increasing tubular pressure, resulting in poor elimination
of sodium, water and metabolic waste.
Nephrotoxic drugs such as aminoglycoside antibiotics,
non-steroidal anti-inflammatory drugs and toxins from
bacteria destroy tubular cells.
The damaged tubular cells become permeable to water,
sodium and metabolic waste.
100. Post renal
Post renal failure results from obstruction along the
ureters, urinary bladder and urethra.
Obstruction resulting from stones in the ureters,
prostatic hyperplasia and urethral stricture could
restrict urine flow, leading to postrenal failure.
110. CHRONIC RENAL FAILURE
DEFINITION - ) CRF is defined as the progressive
reduction in renal function over months to years.
The condition is irreversible and eventually affects all
the organs of the body.
The parenchyma and the nephrons are destroyed and
the renal function progressively diminishes.
111. Etiology
There are many causes for CKD
renal disease such as polycystic disease
arteriosclerosis
chronic glomerulonephritis
chronic pyelonephritis
tuberculosis of the kidneys
diabetes nephropathy
hypertension
renal calculi
prostatic hypertrophy.
