Pathophysiology summary 2nd exam lecture Done by :abeer dirawi & ahmed alshamary & oday noa'man & hadeel sumrain ]السنة[ samsung ]اكتب اسم الشركة[ ]خلتاراختر ا[

93084257 pathophsiology-summary

Embed Size (px)

Citation preview

Page 1: 93084257 pathophsiology-summary

Pathophysiology summary

2nd exam lecture Done by :abeer dirawi & ahmed alshamary & oday noa'man & hadeel sumrain


samsung ]اكتب اسم الشركة[ ]اختر التارخ[

Page 2: 93084257 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


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.

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.

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: 93084257 pathophsiology-summary

Alpha 1 :blood vessel


Alpha 2 : heart vasodilatation

Beta 1 : increase heart rate &


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: 93084257 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.

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 )

Page 5: 93084257 pathophsiology-summary

We can classify the factors which cause hypertension into two


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


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 HR

3. Calcium antagonist – reduce HR & relax BV

4. 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


Done by: Abeer dirawi.

Page 6: 93084257 pathophsiology-summary

lec. summary Heart Failure

Definitions occur 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



Valvular Heart Disease Congenital Heart Disease

Alcohol and Drugs. Arrhythmias

Ventricular Dilatation. Myocyte Hypertrophy.

Salt and Water Retention. Sympathetic Stimulation.

Peripheral Vasoconstriction.

Page 7: 93084257 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 HF



Elevated Jugular Venous Pressure



Bi-basal crackles – in the lungs

Pleural effusion

Ankle Edema


Tender hepatomegaly

Classification of heart failure

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

physical activity."

Category Symptoms

No limitation. heavy exercise

Mild limitation normal physical activity

Marked limitation gentle physical activity

Page 8: 93084257 pathophsiology-summary

Kussmaul’s sign Seen in

1-constrictive pericarditis

2-right heart failure

3-right ventricular infarction

4-tricuspid stenosis

5-restrictive cardiomyopathy

6-"VIP" tamponade + degree of constricive pericardiditis

Kussmaul’s sign Not Seen in

1- 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 Name Time

S1 Close of AV valve

S2 Close of Semilunar valve

S3 "Pathological after 40" Start of Diastole

S4 "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: 93084257 pathophsiology-summary

To do Compensatory mechanism

Increased HR




-Frank Starling

- Contractility


Redistribution of

Blood to the Brain


Vicious cycle will -Decrease in cardiac output

-The body demand for more


in the afterlaod TPR + Increase

Increase in the preload COP

more and more lead to

deteriorated of the heart !


People who developed acute

pulmonary edema , should have

endotracheal, To get rid of

excessive fluid

Page 10: 93084257 pathophsiology-summary

Treatment of HF !

1. Diuretics .

2. Beta blockers . (Decrease CO)

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


- 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. Confusion

3. Discoloration, the patient will have yellowish discoloration

4. Loose of consciousness


-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


Ahmed Al-Shamary

Note About Viagra

- general vasodilator

- Cause Tachycardia

- Fatal for Old people

Page 11: 93084257 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


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 soon

o 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: 93084257 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 :

Page 13: 93084257 pathophsiology-summary

Urine Formation by the Kidneys:

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 )

Page 14: 93084257 pathophsiology-summary

Hematuria Proteinuria

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


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


3-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


5-Apperes in hypertention and

diapetus maletuas.

Done by: Oday noa'man.

Page 15: 93084257 pathophsiology-summary

Cause Kind of anemia

Due to deficiency of iron. Either by : a-loss of iron because of bleeding. b-inadequate iron intake. c-malabsorption. D- parasites.

1-iron deficiency anemia.

Due to deficiency of vit.B12 and /or folic acid. By: a-inadequate intake. b-IF deficiency(for vit.B12) c-diseases of terminal ileum(site of vit.B12 absorption) D-parasites. e-malabsorption (folate is mainly absorbed in jejunum) f- increase demand for folic acid.

2-megaloblastic anemia.

Due to failure or reduction in the ability of the bone marrow to produce RBC's. the cause is either idiopathic, or because of :a-bone marrow inhibition by drugs. b-chemical effect. c-radiation. D- disease ex.viral hepatitis.

3-Aplastic anemia.

Associated with chronic diseases due to the inhibitory effects of cytokines on iron metabolism or erythropoiesis process.

4-Anaemia of chronic diseases.

Due to excessive destruction of RBC's. either congenital :a-RBC membrane abnormalities . b- haemoglobinopathies. c-RBC's enzyme defect. OR..acquired: a- immune disease. b- non- immune :*mechanical causes . *infections. *drugs & chemicals. *malaria.

5-Haemolytic anemia.

Inheritance autosomal recessive trait. 6-Sickle cell anemia.

"G6PD" is important to generate "NADPH". 7-Anemia due to deficiency of (G 6 P D).

Page 16: 93084257 pathophsiology-summary

مقارنة بن الصداع العادي ..والصداع النصف ..

ه تفسر بعض االشاء.. 7اوال ..ف سالد

Has two of the following..

عن عشان نحك انه صداع نصف الزم كون عنا على االقل اثنن من هذه

االعراض ..

1-unilateral location..

بكون بجهة واحدة اما بالمن او السار.

2-pulsating quality..

عن االلم زي النبض بروح وبج .

3-severe intensity..

الم حاد.

4-aggravated by activity..

بزد مع القام بالنشاطات "العمل".

Tension headache migraine

bilateral Unilateral

constant Pulstating quality Not severe Severe intensity

Do not Aggravate by activity Aggravated by activity

Not Associated with vomiting or photophobia/phonophobia

Associated with vomiting or photophobia/phonophobia

Photophobia:.نزعج من الضوء

Phonophobia: نزعج من الصوت العال

Page 17: 93084257 pathophsiology-summary

Test your self

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

or 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 18: 93084257 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