Pathophysiology summary
2nd exam lecture
Done by :abeer dirawi & ahmed alshamary & oday noa'man & hadeel sumrain
samsung ][ ][
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.
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
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. 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 Beta 1 : increase heart rate & contractility
The vein affected by the sympathetic system more than any other blood vessels because they are blood reservoir .
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 ).
Ischemic heart disease Myocardial infraction Stroke Congestive heart failure Kidney failure Heart attack Heart rhythm problems Aneurysm (localized, blood-filled
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 its not treated it will be fatal - resistant doesnt respond to treatment of three medications
Definitions
occur together
Heart Failure The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body.
Valvular Heart Disease Congenital Heart Disease Alcohol and Drugs. Arrhythmias Ventricular Dilatation. Myocyte Hypertrophy. Salt and Water Retention. Sympathetic Stimulation. Peripheral Vasoconstriction.
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 Signs: 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." Category No limitation. Mild limitation Marked limitation Symptoms heavy exercise normal physical activity gentle physical activity
Note that ! Kussmauls sign Seen in an increase in jugular 1-constrictive pericarditis venous pressure and it is 2-right heart failure a sign of Right side heart 3-right ventricular infarction failure . 4-tricuspid stenosis 5-restrictive cardiomyopathy 6-"VIP" tamponade + degree of constricive pericardiditis Kussmauls sign Not Seen in 1- acute cardiac tamponade
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 S1 S2 S3 "Pathological after 40" S4 "always Pathological " Time Close of AV valve Close of Semilunar valve Start of Diastole After Aerial Contraction
To do Compensatory mechanism
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
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 isnt a safe drug the therapeutic index of it is narrow
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
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 RBCs in urine ) Proteinuria ( presence of abnormal concentration of proteins in urine )
Hematuria 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.
Proteinuria 1-Normally low molecular weight proteins are filtered at the glomeruli. 2-Normally albumin ( has a high M.W ) is not filtered at glomeruli 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 hypertension.
6-Red urine can sometimes be 5-Apperes in hypertention and due to other reasons like food dye diapetus maletuas. or drugs.
Kind of anemia
1-iron deficiency anemia.
Cause
Due to deficiency of iron. Either by : a-loss of iron because of bleeding. b-inadequate iron intake. c-malabsorption. D- parasites. 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. Due to failure or reduction in the ability of the bone marrow to produce RBC's. the cause is either idiopathic, or because of :abone marrow inhibition by drugs. bchemical effect. c-radiation. D- disease ex.viral hepatitis. Associated with chronic diseases due to the inhibitory effects of cytokines on iron metabolism or erythropoiesis process. 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. Inheritance autosomal recessive trait.
2-megaloblastic anemia.
3-Aplastic anemia.
.. .. .. .. 7 Has two of the following.. .. 1-unilateral location.. . 2-pulsating quality.. . 3-severe intensity.. . 4-aggravated by activity.. ." "
migraine
Unilateral Pulstating quality Severe intensity Aggravated by activity Associated with vomiting or photophobia/phonophobia . Photophobia:
Tension headache
bilateral constant Not severe Do not Aggravate by activity Not Associated with vomiting or photophobia/phonophobia
Phonophobia:
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 .
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