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Pathophysiology summary 2nd exam lecture Done by :abeer dirawi & ahmed alshamary & oday noa'man & hadeel sumrain [ ة ن س ل ا] samsung [ كة ر ش ل ا م س ا ب ت كا] [ خ ير ا ت ل ا ر ت خا]

Pathophsiology Summary

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Page 1: Pathophsiology Summary

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Pathophysiology summary2nd exam lecture

Done by :abeer dirawi & ahmed alshamary & oday noa'man & hadeel sumrain

Page 2: Pathophsiology Summary

First lecture Summary

Right and left side of the heart are separated from each other by fibrous tissue .There are two opening in the heart in the fetal life and should be closed after birth : 1-foramin ovali. 2-ductus arteriosus.

The impulse transmit in the heart by the conductive system not direct between the atrium &ventricle ,except in rare situation called muscular bridge.The location of the heart: in the mediastinum between the 2nd -5th intercostal space.PMI= point of maximum impulse "where you can feel the impulse".Cardiomegaly :enlargement of the heart "the PMI will increase ".Papillary muscle: it's the muscle attached to the atrioventricular valves via the chordae tendinae.Arteriole: control blood pressure.Vein: blood reservoir .The heart is self-excited .The heart work not under the direct control of the Brian ,but it's affected by the sympathetic and parasympathetic system.

For your information

ductus arteriosus ,what is it??

In the developing fetus, the ductus arteriosus (DA), is a blood vessel connecting the pulmonary artery to the aortic arch. Upon closure at birth, it becomes the ligamentum arteriosum.

Page 3: Pathophsiology Summary

Atrium innervated mainly by parasympathetic system & ventricle mainly by sympathetic system. The heart is affected by hormones mainly adrenaline and noradrenaline which is secreted by adrenal gland, they cause central vasodilation and peripheral vasoconstriction.

Alpha 1 :blood vessel vasoconstriction

Alpha 2 : heart vasodilatation

Beta 1 : increase heart rate & contractility

Beta 2 : bronchi dilatation

The vein affected by the sympathetic system more than any other blood vessels because they are blood reservoir .

Done by: Hadeel sumrain.

Page 4: Pathophsiology Summary

Hypertension lec. summary

Hypertension : It is sustained blood pressure beyond the normal average .- The normal blood pressure :

- systolic : 120-139 mm- diastolic : 80-89 mm

- BP = diastolic + 1/3(systolic – diastolic )

Regulation of blood pressure :

A. Short term regulation : moment to moment regulation controlled by barrow receptors .

B. Long term regulation: the mechanism to maintain blood volume “there is compensated blood loss” !

Signs & symptoms of hypertension :

“ silent killer “ usually no symptoms but rarely it shows :

- Headache - Blurry vision - Chest pain - Frequent urination at night

Blood pressure measurement :

- Optimal : systolic < 120 & diastolic < 80 - normal : systolic < 130 & diastolic < 85 - high normal : systolic < 130-139 & diastolic < 85 – 89

Causes of hyper tension :

1. Primary hyper tension: which is 90 -95 % of the cases that the cause of it is unknown.

Page 5: Pathophsiology Summary

2. Secondary hypertension , it’s only 5-10% that the cause might be cardiac , renal or endocrine ( these systems involved in the maintenance of blood pressure )

We can classify the factors which cause hypertension into two categories:

a) Controllable factors : increased salt intake , obesity , alcohol , stress, lack of exercise and smoking .

b) Uncontrollable factors : heredity , race and age ( men 35-50 , women after menopause ).

Hypertension may lead to Ischemic heart disease Myocardial infraction

Stroke Congestive heart failure Kidney failure Heart attack Heart rhythm problems Aneurysm (localized, blood-filled balloon-like bulge . in the wall of a blood vessel).

Medications :1. Diuretics – get rid of excess fluids 2. Beta blockers –reduce HR3. Calcium antagonist – reduce HR & relax BV4. Angiotensin II receptors blockers 5. Vasodilators

- malignant hypertension if it’s not treated it will be fatal - resistant doesn’t respond to treatment of three

medications

Page 6: Pathophsiology Summary

Done by: Abeer dirawi.

Heart Failure lec. summary

Definitionsoccur together

Heart Failure

The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body.

Pulmonary Edema

An abnormal accumulation of fluid in the lungs.

Causes of Heart Failure

1-Ischemic Heart Disease

2-Cardiomyopathy

3-Hypertension

Valvular Heart Disease Congenital Heart DiseaseAlcohol and Drugs. Arrhythmias

Ventricular Dilatation. Myocyte Hypertrophy.Salt and Water Retention. Sympathetic Stimulation. Peripheral Vasoconstriction.

Page 7: Pathophsiology Summary

When we need more Blood due to the body demand but at that time we were suffering from HF and low Cardiac Output then the Heart will do the Following

1-Sympathetic stimulation ( lead to #2) 2-Increase in heart rate , contractility ,cardiac output .3-Release/formation of Angiotensin II to increase of the volume.4-Vasoconstriction (Increase in the after load ) 5-Increase in the heart size (cardiomegaly )

How can we discover that we have HFSigns:

Cardiomegaly Elevated Jugular Venous Pressure Tachycardia Hypotension Bi-basal crackles – in the lungs Pleural effusion Ankle Edema Ascites Tender hepatomegaly

Classification of heart failure" Symptoms of HF occur at rest and are exacerbated by any

physical activity."

CategorySymptomsNo limitation.heavy exerciseMild limitationnormal physical activity

Marked limitationgentle physical activity

Page 8: Pathophsiology Summary

Kussmaul’s sign Seen in

1-constrictive pericarditis2-right heart failure3-right ventricular infarction4-tricuspid stenosis5-restrictive cardiomyopathy6-"VIP" tamponade + degree of constricive pericardiditis

Kussmaul’s sign Not Seen in1- acute cardiac tamponade

What is PMI and Where ?is the furthermost point outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt.

PMI is at left 5th intercostals space, at the point of intersection

with the left midclavicular line.

PMI Abnormalities! 1- Dextrocardia, the apex beat may be felt on the right side. 2-Cardiomegaly , enlargement of the heart (at the 6th or 7th intercostals space).

Heart Sound NameTime

S1Close of AV valveS2Close of Semilunar valve

S3 "Pathological after 40"Start of DiastoleS4 "always Pathological "After Aerial Contraction

Note that! an increase in jugular venous pressure and it is a sign of Right side heart

failure.

Page 9: Pathophsiology Summary

To do Compensatory mechanism

Increased HR-Sympathetic-Norepinephrine

Dilation-Frank Starling -Contractility

Neurohormonal Redistribution of

Blood to the Brain

NOTE THAT !Vicious cycle will

-Decrease in cardiac output

-The body demand for more

ALSO,

Increase in the afterlaod TPR + Increase in the preload COP

lead to more and more deteriorated of the heart!

ALSO,

People who developed acute pulmonary edema , should have endotracheal, To get rid of excessive fluid

Page 10: Pathophsiology Summary

Treatment of HF !

1. Diuretics . 2. Beta blockers . (Decrease CO)

3. ACE inhibitors (both preload and afterload will decrease .)

Digoxin- increase the force of contraction by increase the Ca concentration in the myocytes and decrease the HR. - Digoxin isn’t a safe drug the therapeutic index of it is narrow

- Digoxin toxicity: High amount of the Drug

Leads to 1. Dizziness.2. Confusion3. Discoloration, the patient will have yellowish discoloration4. Loose of consciousness

Treatment: -Digoxin immune fab -antidote for Digoxin

What is Cyanosis!It is the Blue discoloration of skin and mucus membranes, we can see it in the patient who has heart failure.

We Can't treat the acute pulmonary edema by chest tube there is no air or fluid in the pleural cavity(cover the lung)

excessive fluid usually are absorbed.

Done By Prince

Ahmed Al-Shamary

Note About Viagra -general vasodilator

-Cause Tachycardia -Fatal for Old people

Page 11: Pathophsiology Summary

arrhythmia lec. Summary

Arrhythmia :abnormality in the conductive system of the heart.The SA node is the pacemaker of the heart where the impulse should be initiated ,but some time the impulse could be initiated elsewhere in the heart this is called "ectopic beat ". Refractory period : the period of time come after each AP and the heart muscle can't be excited through it because of the inactivation of fast Na channel. Herat block :

o 1-Block at the level of AV node : a- first degree heart block (PR > 0.22 sec.) b- second degree heart block(some P wave conduct ). C-third degree heart block(complete heart block).

o 2- block below the AV node: a- block at bundle of his. b- block at the branches.

Causes :acute MI, calcify aortic stenosis ,cardiomyopathy, drug,ischemia.Tachycardia : the HR more than 100/min (in ECG short PR interval)Bradycardia : the HR is less than 60/min( in ECG prolonged PR interval).The main cause of fibrillation are:

o Strong electrical shock.o Sever ischemic heart disease.

The main cause of AP re-entry :o Long pathway around the circle.o Decrees velocity of conduction .o Shortened refractory period of the muscle .

Premature beat:o Premature atrial contraction:- the P wave occur too soono Premature ventricular contraction:- the QRS complex prolonged .

Ventricular tachy-arrhymia :Decrees in the COP , the ECG is odd shape. Anti-arrhythmic drug:B blockers & Ca or Na channels blockers & digoxin.

Done by : Hadeel sumrain.

Page 12: Pathophsiology Summary

The kidney lec. summary

Review of kidney structure and function

Functions of the kidneys :

excretion metabolic waste products ( Urea , Uric acid , Creatinine and Bilirubin )

e xcretion foreign chemicals ( Food additives , toxins , pesticides , drugs )

secretion , metabolism & excretion of hormones ( Renal erythropoietic factor, Renin and 1,25 dihydroxycholecalciferol )

Regulation of erythrocytes production

Regulation of vitamin D activity (Vitamin D3 is important in calcium and phosphate metabolism )

Gluconeogenesis ( synthesis of Glucose )

Regulation of acid-base balance

Regulation of arterial pressure ( Endocrine Organ and Control of Extracellular Fluid Volume. )

Regulation of water and electrolytes balances:

And these functions are acomplished by a sereis of processes like

Filtration , reabsorption , Secretion and Excertion of urine

Very Important note :

Urine Formation by the Kidneys:

Page 13: Pathophsiology Summary

Glomerular Filtration

Renal Blood Flow, The functional unit of the kidney is the Nephron the reabsorption and the secretion happened between the pretubular

capillaries and the tubules Filtration occurs between the glomerulus and Bowman's capsule

Filtration: not selective (except for proteins), averages 20% of renal plasma flow

Excretion = filtration – reabsorption + secretion

Reabsorption: highly variable and selective

We have 3 layers glomerulus ( a network of capillaries ) :

1-Epithelium of the glomerulus 2-Basement membrane 3-Endothelium Wall of bowman's capsule ( consists of non-dividing epithelial cells ( podocytes ) )

Pathophysiology of the renal system

1-Disorders of urine volume ( Anuria , Oliguria and polyria )

2-Disorders in urine composition Hematuria ( blood od RBC’s in urine ) Proteinuria ( presence of abnormal concentration of proteins in

urine )

Hematuria Proteinuria

Page 14: Pathophsiology Summary

1-Glomerular bleeding suggests fracture in the GBM.

2-Glomerular bleeding may develop after strenuous exercise.

3-Recurrent episodes of gross hematuria associated with respiratory tract infection indicates IgA nephropathy .

4-Glomerulonephritis with deposition of IgA in mesangial cell.

5-Red urine due to haematuria must be differentiated from other causes of red or black.

6-Red urine can sometimes be due to other reasons like food dye or drugs.

1-Normally low molecular weight proteins are filtered at the glomeruli.

2-Normally albumin ( has a high M.W ) is not filtered at glomeruli3-Minor leakage of albumin into glomerular filtrate may occur temporarily after vigorous exercise fever and heart disease.

4-Albuminuria is seen in early stages of glomerular disease of diabetes mellitus "diabetic nephropathy " also in hypertension.

5-Apperes in hypertention and diapetus maletuas.

Done by: Oday noa'man.

Page 15: Pathophsiology Summary

Test your self

Q)the impulse in the heart conduct directly between the atrium and ventricle, True or false?

A-false.

Q)in normal person the PMI should be on which intercostal space?

A- on the 5th intercostal space.

Q) what will happen if one of the papillary muscles get ruptured?

A-the blood will back to the atrium and that will reduce the output of the heart.

Q)The resting coronary blood flow equal?

A- 225 ml/min

Q) The perfusion occurs during the systole , True or false?

A- False, during diastole.

Q) if the metabolic regulation increase then the blood flow will?………

A- increase.

Q) sympathetic stimulation increase the heart rate and contractility and decrees the cardiac output , True or false?

A- false, "increase the cardiac output. "

Q) when there is a complete occlusion of the coronary artery this will lead to necrosis . necrosis is less severe than ischemia ,true or false?

A- 1- True . -2- false .

Q) The location of the obstruction do not affect the quantity of myocardial ischemia, true or false?

A- false.

Q) What do we mean by " ectopic beat? "

A- it's an abnormal case when the impulse of the heart initiated not in the SA node but elsewhere.

Page 16: Pathophsiology Summary

Q)regarding Refractory period why the heart muscle can't be excited through it?

A- because of the inactivation of fast Na channel.

Thanx alooot for :Abeer dirawi & Ahmed Al shamary & Oday noa'man ..

the best of luck