Schemes

Schemes of Pediatrics NMT10
Cardiology scheme
Congenital Heart Disease
Definition:
Etiology:
1. Idiopathic: Most common cause
2. teratogenic Drugs in 1st 3 months of pregnancy
- e.g.: Aspirin All congenital Heart except Patent Ductus
- e.g.: Warfarine Lithium carbonate(antidepressant)
3. Irradiation.
4. Congenital Infections TORSCH.
-e.g.: Rubella Patent Ductus
5. Chromosomal Disorders:
-e.g.: Downs syndrome Common A.V canal
Trisomy 13 Midline defects(ASD,VSD,PDA)
Turners Coarctation of aorta
Nonan syndrome pulmonary stenosis
Marfans syndrome Aortic incompetence
6. Maternal Diseases:
- e.g.: Diabetes uncontrolled(as monosaccharides can pass throw placenta causing
fetal hyperglycemia &so multiple congenital anomalies) -SLE
7. Gene factor: Common in certain families
Multifactorial inheritance
Clinical Picture:
A- Complaint
very very important:
1.Asymptomatic Accidentally discovered
2.Congestive Lung symptoms:
Plethora ( Rt )
Congestion ( Lt )
- Dry cough(cong of alveolar wall)
- Expectoration(cong of mucus membrane)
- Dyspnea(++ heart rate due to hypoxia)
- Orthopnea
- Paroxysmal nocturnal dyspnea(dominant parasympathetic & so
,bronchospasm)
- Hemoptysis

3.Palpitations: awareness of Heart beats
- Change power of contraction or heart rate
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4.Low C.O symptoms: Anaemia & Oliguria
- Oliguria
- Easy fatigue
- Pallor
- Syncopal attack
5.Cyanosis Central
- Non oxygenated Blood More than 5mg/dl in tongue Potential cyanosis
...

B- Examination:
When Lt ventricle enlarged -Apex shifted down & out Localized Apex
When Rt ventricle enlarged -Pericardial Bulge(take along time)
-Apex shifted out ONLY Diffuse Apex
-Lt Parasternal & epigastric pulsations
When Biventricular Enlarged -Apex shifted Down & Out Diffuse Apex
- Lt Parasternal pulsations
When Lt atrium enlarged(most posterior chamber) -Dysphagia
When Rt atrium enlarged - Rt parasternal pulsations
Pulmonary HTN Pulmonary area
Aortic Aneurysm A1 Systemic HTN
1. Inspection & Palpation:

o Shape
o Apex Site, Type & Character
o Pulsations
N.B.:
-
Apex of the Heart:

< 2 years present in Lt 4th Space OUTSIDE MCL
2-7 years present in Lt 4th Space At MCL
> 7 years present in Lt 5th Space INSIDE MCL
2. Percussion of Heart:
Tidal Percussion
1. Rt border of the Heart:
Parallel to the Sternum
- If any dullness detected Rt Atrial Enlargement
2. Aortic area & Pulmonary area:

If any dullness detected Dilated vessels
If over pulmonary area diastolic shock
3. Outside the apex:

- If any dullness detected Pleural or Pericardial effusions
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3. Auscultations of Heart:
o Heart Sounds
o Murmurs
o Additional Sounds
A. Heart Sounds S1 & S2 (S1 with Carotid Pulsations)
B. Murmurs Timing- Character- Site of Maximum intensity - Propagation
C. Additional Sounds

Heart Sounds:
S1 - Closure of A.V valves
- felt with carotid pulsations
- Better heard on Apex Mitral & Tricuspid Areas
S2 - Closure of Aorta & Pulmonary valves

- Better heard on Aorta 1 Component & pulmonary
2 component
areas
Murmurs:
- Turbulence of Blood flow
- Characters Harsh Soft Rumbling
Complications:
1. Repeated Chest infections:
- All Diseases except Fallots Tetralogy COI associated Pulmonary stenosis
2. Heart Failure:
- All Diseases except Fallot Rare
3. Infective Endocarditis:
- All Diseases except Fallot & ASD Rare
4. Stunted Growth especially Height(as a chronic illness)
5. In cases of Shunt Reversal of Shunt
Central Cyanosis Esinmenger
Investigations:
1. X-ray Chest & Heart: Cardiomegally- Which Chamber Lung Vasculature
2. ECG
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3. ECHO cardiography
4. Diagnostic cardiac catheterization
Treatment:
1. Medical: Prophylaxis against Infective Endocarditis
2. Surgical: Correction
Hematology scheme

Acute Hemolytic Anaemia Intravascular Hemolysis
Chronic Hemolytic Anaemia Extravascular Hemolysis

Life Span of RBCs : 120 days

Bone Marrow can increase its capacity 8 times more lead to:
- Long Bones Fragile Bones Medulla & Cortex
- Flat Bones Atrophy of outer cortex Fine Trabeculae makes
Hair on end appearance
- Skull circumferences Macrocranium
Chronic Hemolytic Anemia

Etiology:
a. Intrinsic causes in RBCs:
- Cell mm e.g.: Spherocytosis
- Hb e.g.: Thalassaemia Sickle cell anaemia
- Intracellular enzymes e.g.: G6PD enzyme
b. Extrinsic causes:
- Ab from mother e.g.: RH-ABO
- Autoimmune
RBCs Destruction Spleen Hb

Heme
Iron PPT
Protoporphyrin
Globin Ptn
Protoporphyrin Indirect Billirubin Liver Direct Billirubin Bile

Intestine Commensals Stercobilinogen
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Clinical Picture:
1. Mongoloid facies:
- Due to Hyperactive BM that can increase its ability 8 times more than normal to
produce RBCs leads to Medulla expansion make:
o Prominent Maxilla
o Depressed nasal bridge
o Protruding central incisors
2. Pallor + Manifestations of anaemia:
- Headache
- Lack of concentration
- Dizziness
- Syncopal attacks
- Easily fatigue
- Muscles cramps
- Chest Pain
- O2 Angina
3. History of repeated Bl. Transfusion:
- Since Birth Spherocytosis
- At 6 months Beta Thalassaemia
4. Mild Jaundice:
- Liver can increase its activity 6 times more than normal
- But Beyond this, part of Indirect Billirubin increase & make Mild jaundice which
becomes deep when liver is affected.
5. Splenomegaly: Iron Deposition
- Because spleen becomes the site of RBCs production as well as RBCs
destruction Also, Hepatomegally can occur.
6. Dark colored urine & Stool:
- Dark urine Direct Billirubin Urobilinogen
- Dark Stool Direct Billirubin Stercobilinogen
Complications:
1. Pathological Fractures more than expected for mild trauma:
- COI Bones become more fragile.
2. Complications of frequent Bl. Transfusion:
- Hepatitis B & C
- May be HIV
3. Hypersplenism:
- Due to increase RBCs destruction manifested by:
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o Frequency of Bl. transfusion
o Purpuric eruption Platelet destruction
o Recurrent infection WBCs destruction
4. Traumatic rupture of spleen:
- Due to Splenomegaly.
5. Iron intoxication: Hemosidrosis
- Rapid destruction of RBCs Release of large amount of iron that is ppt in many
tissues causing:
a. Skin Dark pigmentations
b. Heart Cardiomyopathy ms. Weakness
c. Liver & Spleen Enlargement
d. Pituitary gland Hypofunction Short stature & Delayed puberty
e. Islet of Langerhans Diabetes called Bronze Diabetes
Skin become Bronze in color due to mixture of:
Pallor & Jaundice & Hemosidrosis
So, its called Bronze Diabetes
6. Bile Stones:
- Due to increased Direct Billirubin obstruct Bile duct, manifested by:
o Tea colored urine
o Clay colored urine
7. Heart Failure:
- Anemic HF
- Due to Hemosidrosis Cardiomyopathy
8. Crises:
o Megaplastic crises:
- Hyperactive BM needs Iron, B12, Folic acid
Iron: already excess
Vit B12: Dietary Supplement
Folic acid: must be given to patient
o Aplastic crises:
- Bone Marrow arrest
o Hyperhemolytic crises:
- Increase Hemolysis due to G6PD deficiency
Intravascular + Extravascular Hemolysis
o Sequestration crises:
- Spleen enlargement with full sinusoids
9. Infections by capsulated organisms:
- After Splenectomy H influenza- Pneumococci- Meningiococci
Long acting penicillin "

# $%
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N.B.: Long acting penicillin is useful in
Lung Congestion in HF
Aplastic Crises WBCs
Investigations:
1. CBC:
a. Type of Anaemia Normocytic Normochromic in All Hemolytic anaemias
Except in Thalassaemia.
N.B.: Microcytic Microchromic Anaemia in Iron Deficiency anaemia
Thalassaemia -Sideroblastic
2.
3.
4.
5.
6.
7.
b. Abnormal Cells Anisocytosis Target Cells

Serum Iron: Increased
Iron Binding capacity: Decreased
Serum Billirubin: Increase INDIRECT Billirubin But NOT more than 5 mg/dl
Urine analysis: Increase Urobilinogen
Stool analysis: Increase Stercobilinogen
X-Ray:
o Long Bones Wide Medulla & Thin Cortex
o Skull Hair on end appearance
Acute Hemolytic Anemia

Intravascular Hemolysis
Exposure to agent:
-
" & ( RBCs Hemolysis"

Cause HB release in circulation Fever & Rigors
Has pyogenic effect
Kidney Tubules Irritation Loin Pain + Red colored urine
Complications:
-
Can cause Acute Renal Failure
Investigations:
1. CBC:
o Anaemic type: Normocytic Normochromic anaemia
o Reticulocytes
o Abnormal cells Heinz bodies
2. Urine analysis: Hb
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Neurology scheme

Motor system
Sensations
ANS
Other specific findings
Motor system
1.
2.
3.
4.
5.
Muscle Power.
Muscle Tone.
Deep tendon reflexes & Superficial reflexes.
Muscle State.
Distribution & which group of muscles(uni- or bi-lateral ,
proximal or distal , uni- or hemi- or para- or quadric-plegia)
6. Symmetrical or Asymmetrical In Bilateral Lesions
7. Onset of Disease.
8. Course of Disease.
UMN area 4 Cerebellum Basal Ganglion.

LMN Cranial Nerves Spinal Nerves.
1. Muscle Power:
-
Weakness or Paraplegia.
2. Muscle Tone:
-
All times, Muscles are stretched Stretched between its origin & insertion
Stimulate A.H.C always.
3. Deep tendon reflexes & Superficial reflexes:

-
Taping by the hummer on the tendon more stretching of muscle spindles

Stimulate A.H.C Active Contraction.
By this reflxexes we can differentiate between LMNL(hyporeflexia) and
UMNL(hyperreflexia)
4. Muscle State:
-
Autonomic N. S
Arterial blood supply of the muscle

Lower Motor Neurons L.M.N
In LMNL: Vascular flow to muscles Muscles Wasting or pseudo-hypertrophy
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Leveling of Lower Motor Neuron Lesion?
1. Sensations
2. EMG
3. Nerve Irritation
Anterior Horn Cells

Intact
Neuropathic
Or Denervated
normal
Peripheral Nerves
Lost
Neuropathic
Or Denervated
impaired
N-M Junction
Intact
Myopathic
Conduction Velocity
Anterior Horn Cell Lesions - Poliomyelitis
- Spinal ms atrophy
Type I WHD
Type II Late Infancy
Type III Childhood
Type IV Cranial Nerves
- Amyotrophic lateral sclerosis

Peripheral Nerve Injuries - Guillian Bare
- Trauma Birth Injuries: Erbs
- Congenital insensitivity to pain
- Vit B complex, Diabetes, Leprosy
Muscle Disease - Congenital- Endocrinal
Myopathy
Hypothyroidism ATP
Hyperthyroidism ptn ms
Hyperparathyroidism
Cortisone
- Inborn error of metabolism Glycogen storage disease

- Inflammation Dystrophies
N-M Junction Myasthenia Gravis Botulism
N.B: Enumerate causes of peripheral neuritis & discuss how to diagnose one of
them
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Guillian Bare Syndrome

I.
Def.:
Etiology:
Clinical Pic.:
Motor System
1. Ms. Power:
2. Ms. Tone:
3. Tendon
Reflexes:
4. Ms. State:
5. Distribution:
Weakness or Paraplegia
Hypotonia
Hyperreflexia
Ms. Atrophy
Bilateral , Symmetrical , ,./ 1
-Infant More in Distal ms. Than
Proximal ms.
,2 34, 5

-Adult More in Proximal ms. Than
Distal ms(radiculopathyaffect
roots which is nearer to proximal ms)
6. Onset:
7. Course:
Acute
L.L Trunk U.L Bulbar Resp.
Sensations 6 4 7 34, 15 8 65 7 9$1$
Ascending Paralysis
Lost
also
More
in
Distal
Than
Proximal
II. Sensations:
Gloves & Stocking Hypoesthesia
1.Parasympathetic: HTN- Tachycardia- urine retention
III. Autonomic
Hypotension- Bradycardia- Urine
2. Sympathetic:
Nerve Fibers:
incontinence
So, it is Labile Autonomic Manifestations
Encephalo-myeloradiculopathy carnialis
VI. Special
No Myelin ,% CNS &
Findings:
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Juevinillie Myasthenia Gravis

Def.:
Etiology:
Clinical
Picture:
Test:
Investigations:
Treatment:
Easy Fatigability on repetition of muscular activity improved

by Neostigmine or Physostigmine Choline Esterase Inhibitor
Autoimmune antibody against Acetyl Choline when released in
N-M junction
1. Ocular Affection Ptosis-Squint- Diplopia
2. Bulbar Affection Nasal regurge- Dropping of jaw
3. Sudden Paralysis With activity Hypotonia- Bilateral
symmetrical Misdiagnosed with Physic Disorders
associated with Thyroid disease
o Induction of Ms. Fatigue:
Then give Neostigmine Fatigue Disappear
o Walkers Test:
Made by cuff of Sphygmomanometer raise above systole &
induce activity in hand till become fatigued on removal
of cuff , Ptosis appear
1. EMG: Power of ms. Contraction till become flat
2. Anti Acetyl Choline Ab screening
Neostigmine or Pyridostigmine + Plasma Pharesis
o Motor area 4

o Motor area 6
o Basal Ganglion
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Motor Area 4
1. Initation of voluntary movements
-Small muscles of hand & Proximal muscles
2. Suppress ms. Tone & Deep tendon reflexes <
-More to Antigravity ms. Flexors of UL & Extensors of LL &
Adductors > Abductors
3. Suppress Pathological Reflexes 65
-Moro & Grasp reflexes- Jaw reflex Clonus Adductor reflexes(normally all of
them disappear after 4 monthes due to myelination of nerves)
Motor Area 6
-
Proximal Muscles . Not Distal

When motor area 4 is affected, the followings occur: Spastic C.P
- Clasp Knife Rigidity: Resistance at 1st ONLY Irritation =, "5
o Paralysis or weakness of the muscles.
o Distal > Proximal
o Hypertonia in the form of Clasp knife rigidity & Hyperreflexia more in
the antigravity muscles Flexors of UL & Extensors of LL &
Adductors(causing scissoringof l.l.)
o Appearance of Pathological reflexes
o Monoplegia (one limb)
o Hemiplegia (2 limbs,one upper and one lower of the same side)
o Paraplegia (2 u.l or 2 l.l.)
o Quadriplegia Diplegia L.L > U.L
Biplegia U.L > L.L
Cerebellum

Arch cerebellum connected to Cochlea of the inner ear Drunken Gait

Piliocerebellum Stimulate muscle tone & reflexes of antagonist muscles
3%, # 4
% 35

Neocerebellum
o Dysmetria ! # %& ) (
o Decomposition of movement *
( * % , &*-

o Rebound 85,
o Nystagmus Kinetic Tremors Contraction of Agonist &
Antagonist ms. together
o Dysdiadokokinasia Inability to do repeated Supination &
Pronation
Manifestations of Cerebellar affection???
Drunken Gait: Arch cerebellum
Hypotonia & Hyporeflexia: Piliocerebellum Not associated with weakness
Dysmetria & Decomposition of Movement & Nystagmus
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Basal Ganglion
Emotions & associated Movements ...

!
Mask face- No arm swinging with movement Emotional instability
Control abnormal activity of the Motor area 4 during rest "#$ %&' (
Static Tremors- Chorea-Dystonia Movement of the trunk Athetosis Twisting movement of extremies
Control ms. Tone according to Neurotransmitters
Mediators of the basal ganglia

Acetyl Choline: Stimulation
Dopamine: Inhibition
Short stepping shuffling gait
Intracranial Hypertension
-
Headache
Projectile vomiting not perceeded by nausea
Diplopia
Blurring of vision
Acute:

Meningitis & Encephalitis Infection

Encephalopathy HTN Edema & Hemorrhage
Meningism
Chronic: X-ray Silver Needle

-
Craniostenosis Premature closure of sutures

Pseudo
Hypervitaminosis A & D
Space occupying lesion: Tumour- Abscess- Hematoma
Inability to Walk
Paralytic causes
Written (
Non Paralytic causes
Physiological delay Lulls Phenomena

- Delayed Speaking but Early sphincter control
- Delayed Dentition but Early Walking BC
Rickets: Delayed walking- Dentition
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Painful condition: Fracture bones- Arthritis- Scurvy- Dislocation Hip

Severe chronic illness: Marasmus- Kwashiorkor
Myocitis
All above causes are TRANSIENT
All UMNL & LMNL C.P- Hydrocephalus Meningitis

Polio- Werding- Guillian Bare Syndrome Myasthenia gravis
All above causes are PERMENANT
Can be Transient by ttt
Primary Inability to Walk

-
Physiological
Rickets
Polio
Werding Hoffman
Secondary Inability to Walk

-
Painful condition
Polio
Guillian Bare syndrome
Duchene
Juvenile Myasthenia gravis
ORP
Boutulism
Cushing
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Respiratory scheme
Complaint: (In a chronological manner)
a) Cough:
- Dry
- Productive (expectoration)
b) Dyspnea: if chest troubles O2 saturation & Co2 Irritation of respiratory
center respiratory rate E
c) Noisy respiration
d) Chest pain
e) Hemoptysis
f) Wheezes
g) Cyanosis F G4 3 5 ,HI G4 9CJ
Audible sounds: (Noisy respiration)

- Sounds heard by naked ear , heard in partial airway obstruction (not complete)
- Upper respiratory obstruction occur mainly in inspiration
- Lower respiratory obstruction occur mainly in expiration
N.B
Upper respiratory system Nose, mouth , nasopharynx & larynx

Connecting system Trachea & main bronchi
Lower respiratory system Bronchi inside lung , medium sized bronchioles ,
small sized bronchioles & alveoli
LRT
URT
LRT
During
inspiration
C.S
During
expiration
LRT
%,K J $8%
& 1J $8%
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(1) Snoring(INSPIRATORY): defect in nose or nasopharynx (URT)
(2) Stridor (Inspiratory): Partial laryngeal obstruction in inspiration
(3) Wheezes (expiratory): Obstruction in mediam sized or small bronchioles, starts
with expiration then both
(4) Grunting
: Alveolar pathology , maily pneumonia , causing laryngeal
sound , mainly in infants
(5) Rattling: secretion in the collecting system , both inspiration & expiration
N.B
Type I alveolar cells secretes mucous , protect alveoli from any forigen
particles
Type II alveolar cells secrete surfactant surface tension (by alveolar
secretion) & L G4 8 5 $8% $ #
Alveolar pathology: destruction of type II cells surfactant alveolar
collapse & +++ secretion due to inflammation
Protective mechanism comes from larynx: by contraction of adductors of vocal
cords bring cords in midline incomplete expiration by incomplete evacuation
of air from alveoli to prevent their collapse
Full expiration ./ 1& 23 1 % 1 7
( ;./ " $< ) &" . 8/ 9&8/
Lapping > 2 ?
Local examination:
A. INSPECTION:
1- Respiratory distress
2- Chest movement
3- Bulge or retraction
(1) Respiratory distress: (4 grades)
i. Tachypnea & working ala nasi
ii. Accessory muscles or respiratory:
- Intercostals (LRT) Retraction in intercostals & subcostal
To +++ transverse diameter
- Trapezius & sternomastoid (URT)
Retraction in suprasternal & supraclavicular
To +++ vertical diameter
iii. Granting
iv. Central cyanosis (severe respiratory failure)
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(2) Chest movement:
- To Know where is the lesion in unilateral pathology
- All diseases of respiratory system restrict movement except bronchitis
(3) Bulge or retraction:
Bulge
Air: Tension pneumothorax (Pleura G4 ), unilateral emphysema
Fluid: Pleural effusion (masses)
N.B: All types of effusion are unilateral except traumatic bilateral
Retraction: Fibrosis or collapse

9. A Retraction or bulge &bilateral lesion (
Antero-posterior / Transverse diameter ration (Normal = 2/3)
If 1/3 Retraction (flat chest) in bilateral fibrosis or collapse
If 1/1 Bulge (Barrel chest) in massive bilateral effusion (generalized
edema) or bilateral tension pneumothorax or babies which on ventilator or
emphysematous lung (B.A & bronchiolitis & empyema)
B. PALPATION:
1- Position of mediastinum (detected by position of trachea)
2- Palpable sounds
3- Tactile vocal fremitus
(1) Position of mediastinum: centralized, pushed to , attracted to .
- Pushed by (to opposite side) causes of unilateral bulge
- Attracted by (to the same side) causes of unilateral retraction
(2) Palpable sound:
- Wheezes "Ronchi"
- Pleural rub "Dry pleurisy" NF G4 ( 9O
(3) TVF: corporative examination of both sides (Laryngeal sound 44 6 ,)
- by all lung diseases except:
o Consolidation (pneumonia)
o Lobar collapse
C. PERCUSSION:
-
Normal Resonance
Abnormal
1) Hyper resonance: ++ air in pleura or lung
Unilateral or bilateral
Causes of unilateral air bulge e.g. Unilateral emphysema & unilateral
tension pneumothorax
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Causes of bilateral air bulge e.g. Bilateral tension pneumothorax &
emphysematous lung
2) Dullness (impaired note) all other diseases
Stony dullness pleural effusion
D. AUSCULTATION:
1- Air entry
2- Breath sounds
3- Adventitial sounds
(1) Air entry:
- in all diseases except bronchitis
- Detect if there's unilateral pathology
(2) Breath sounds:
a) Vesicular (Normal)
b) Harsh vesicular: all diseases except (Bronchial causes)
- Inelastic alveoli
- Airway Obstruction
- Normal till 1-2 days
c) Bronchial: occur in Pneumonia ( alveoli secretion)
Collapse (no air inside)
Mass
So become solid mass & heard only from near by bronchioles
(3) Adventitial sounds: very very very important table
Crepitations / C.DE
Fine : unhealthy alveolar

wall
e.g. pneumonia , bronchiolitis , acute
congestive HF , Bronchiactasis &
mycoplasma pneumonia
Coarse : air passage through

fluid
e.g. Bronchitis , Bronchiolitis ( if
secretes before cough) , BA , OPC ,
pulmonary edema
- Coarse: changeable acc to secretions
Ronchi #DE C.DE
Sibilant "! :

- If bilateral bronchospasm BA ,
bronchitis , viral pneumonia
If localized FB and also may be:

- Dry secretions
- Compression from outside by LNs
- Sonorous #$%& $': like coarse
crepitations
Complications:
A) Respirator failure: Cyanosis
Laboratory diagnosed by blood gas analysis
PH < 7.2
7.35 _ 7.45
PO2 < 50 mmHg
80 _ 100 %
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PCO2 > 50 mmHg
25 _ 35 %
B) HF due to . Bacterial chest infection Toxic myocarditis
. Viral chest infection Viral myocarditis
. Severe hypoxia Cardiomyopathy
. Core palmonale due to emphysema , fibrosis of lung
Investigations:
A) Chest x-ray
B) CBC . if neutrophils (++ TLC , mainly neutrophils): due to bacterial infection
. If ++ lymphocytes: due to viral infection or TB
. If eosinophils: due to BA (atopy)
C) Bl. Gases to detect if respiratory failure
D) Specific investigations according to every disease
Treatment:
If respiratory distress:
Hospitalization O2 therapy
Complete rest
IV fluids: 2/3 maintanance dose as it prevent hypoxia causes state of
secretion of ADH prevent H2O Loss & preserve it
TTT of etiology symptomatic TTT
TTT of complications
- NaHCO3 acidosis
- Ventilator hypoxia
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Nephrology scheme
Renal Failure
Functions of the kidney:
1. Endocrinal function
2. Excretory function
3. Power of Conc. & Dilatation
1. Endocrinal Function:
1. Erythropoietin formation of RBCs
2. Activation of Vit D, I need 2 OH group one of them from liver at carbon atom &
from 25 hydroxycalciferol, The other OH from kidney to form 1,25
dihydroxycalciferol Active form of Vit D & act as a hormone
3. Release of Renin from Juxtaglomerular apparatus cells at the end of afferent
arterioles it increases Bl. Pr by Renin-Angiotensin system By:
o VC of peripheral vessels Increase resistance Increase Diastolic Pr
o Angiotensin cause release of Aldosterone from suprarenal Salt & Water
retention Hypervolemia Hypertension
If defect of Endocrinal functions:

1. Anaemia
2. Decrease form of Vit D Decrease Mineralization of Bones;
In Old age
Osteomalacia
In Young age Rickets
/0
1
3. If irritative pathology Stimulation of Juxtaglomerular apparatus cells
Increase Renin Increase HTN
4. If Destruction pathology No Renin Hypotension
2. Excretory function:
(Of Waste products)
1. Major toxins; appear early, may be fatal, severe:

o Urea: Most important
o Ptn Ammonia Urea Main Site of Excretion Kidney
o Acidic Materials C5 Bicarbonate 9<# ,Q# So, Urine is Acidic
oK+
oP
2. Minor toxins: Appear late, mild & Not fatal:
o Urochrome pigments
o Phenol
o Aluminum
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If defect of Excretory functions:
Major Toxins:
1.Urea (extremely important): uremia Azothemia RF, Body response is to
excrete it in:
o Saliva:
Not able to taste anything or bad taste or bad mouth odour # G4 L85
o Sweat:
a) Water of sweat evaporize & urea salts remain on skin
Urea Frast , # 8E G8% R # 8 S$ 65 1N
b) Severe itching on any site of sweat Skin rash
o GIT:
a) In stomach secretion cause inflammation of Stomach wall Gastritis
<, # & 3 5 ...7,
3<J, 15
b) In Colon secretion inflammation of the wall of colon Dysentery

Uremia Dysentery
o On peritoneal scar: Dry peritonitis 6"1 & H 7
o Respiratory:
a) Excretion with mucous in bronchus causing bronchus inflammation
Then Wheezes Then Bleeding Hemoptysis
# 6 # T # 6 # U81# 6 #< (
b) Dry Pleurisy
c) Uremic Breathing
o CVS:
a) Heart: Cardiomyopathy HF
b) Pericardium: Dry pericarditis
c) HTN
o Hematology:
a) RBCs: Deformity of Cell membrane Hemolytic anaemia
b) Platelets: Decrease of cyclo-oxygenase enzyme Thrombo-asthenia
c) Cholesterol: Decrease of Lipo-ptn lipase enzyme
Hypercholesterolemia
o CNS: In Advanced cases
a) Irritation of chemoreceptor trigger zone Vomiting
b) Suppression of Reticular formation coma of disturbed level of
consciousness
2.Acidotic material: 1 Retention of it & so 2 Excretion of bicarbonate in urine
metabolic acidosis & alkaline urine.
Metabolic acidosis body try to correct pH by 1 Stimulation of respiratory
center rapid & deep respiration (air hunger) to excrete CO2 (acidic), 2 +++
bicarbonate in blood by release Ca- carbonate from bone (milking of bone)
so (Osteomalacia OR Rickets). /0
1 345
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22 | P a g e

3.Potassium:
Retention acute renal failure (no filtration).
In CRF dec. number of nephrons (no effect on serum K+ except in end
stage renal failure inc. K+).
Tachyarrythmias (by effect of S.A. node).
On smooth muscles (GIT) inc. motility of GIT abdominal colic & dec.
time for absorption diarrhea.
On skeletal muscles dec. muscle tone & power muscles weakness &
hypotonia.
so the action of k on smooth ms is different of thay on skeletal ms. ( !(

)6-
Causes of diarrhea in CRF:

1) Inc. motility due to inc. K+.
2) Uremic dysentery.
3) Gastroenteritis (due to dec. immunity).
4) Gastrocolic reflex (due to gastritis).
Abdominal pain in CRF:

1) Heart burn (gastritis).
2) Dysentery.
3) Inc. motility.
4) Diffuse abdominal pain (peritonitis).
4. Phosphorus: Parathyroid hormone tends always to inc. serum Ca++ & dec.
serum P+ by action on 2 sites:
a) Bone: Activate osteocalst inc. Ca++ & P+.
b) Kidney: Preserve Ca++ (active reuptake) & excrete P+ (active excretion).
N.B
In Renal Failure Destruction of parathormone receptor in kidney
& so inc. Ca++ & dec. P+ in urine & so dec. Ca++ in blood & inc. P+ in blood ,
so inc. parathormone activity in bone release Ca++ may be balanced, but P+
inc. more & more (vicious circle more & more serum P+), so inc.
demineralized areas (osteitis fibrosa cystica), so osteomalacia & rickets.
Therefore, in end stage renal disease low Ca++ level due to exhaustion of bones
but it doesnt cause tetany due to acidosis (prevent tetany).
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23 | P a g e
Minor toxins:
1. Urochrome pigment:
From degradation of melanin pigment, excreted only through urine, giving its
yellow colour.
In Renal failure:
Not excreted in urine causing white colour of urine.
Inc. level of it in blood causing yellow colour of skin (like anemia) but not
improve with blood transfusion give the earthy look colour.
2. Phenol:
Excreted only by kidney.
In Renal failure: inc. in body

Irritation of anterior horn cells causing muscle twitches (fasciculation).
Irritation of phrenic nerve hiccup (30% of R.F cases are diagnosed by
this complaint).
3.
Aluminum: .(9$H 85
K& Z) ,E
& 8<( 1 :T,N 6% &H #
., G4 Q
( & 2
Aluminum toxicity:
Neuropsychiatric disorders depression, anxiety, Alzheimer.
Depression of bone marrow pancytopenia.
3. Power of concentration and dilution:

Specific gravity in renal failure = 1010 (low & fixed). %7
*4 79: ,79( 0

Precautions for measuring (normally):
Fasting (fluid & food) for at least 10 hours ( dec. intake of water & there is
normal loss of water in sweat & C.S.F hypovolemia dec. V.R.
activation of hypothalamus volume receptors release of ADH by
hypothalamus which act on collecting tubules & open H2O channels
medullary suction of H2O from nephrons by osmolarity dec. urine volume
& inc. specific gravity (1030).
Then take 6 cups of juice (1.5 liters) inc. intake hypervolemia dec. ADH
block of H2O channels inc. urine volume & dec. specific gravity (1015).
In renal failure:
Destruction of all receptors plasma come out as urine without any change
Urine specific gravity becomes as plasma (1010).
www.MedadTeam.org
24 | P a g e

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Schemes of Pediatrics NMT10

Schemes of Pediatrics NMT10

1. Inspection & Palpation:

Apex of the Heart:

2. Aortic area & Pulmonary area:

3. Outside the apex:

Schemes of Pediatrics NMT10

S2 - Closure of Aorta & Pulmonary valves

Schemes of Pediatrics NMT10

Life Span of RBCs : 120 days

Chronic Hemolytic Anemia

RBCs Destruction Spleen Hb

 Protoporphyrin Indirect Billirubin Liver Direct Billirubin Bile

Schemes of Pediatrics NMT10

Schemes of Pediatrics NMT10

Schemes of Pediatrics NMT10

b. Abnormal Cells Anisocytosis Target Cells

Acute Hemolytic Anemia

" & ( RBCs Hemolysis"

Kidney Tubules Irritation Loin Pain + Red colored urine

Can cause Acute Renal Failure

Schemes of Pediatrics NMT10

UMN area 4 Cerebellum Basal Ganglion.

3. Deep tendon reflexes & Superficial reflexes:

Taping by the hummer on the tendon more stretching of muscle spindles

Arterial blood supply of the muscle

In LMNL: Vascular flow to muscles Muscles Wasting or pseudo-hypertrophy

Schemes of Pediatrics NMT10

Anterior Horn Cells

- Amyotrophic lateral sclerosis

- Inborn error of metabolism Glycogen storage disease

Schemes of Pediatrics NMT10

Schemes of Pediatrics NMT10

Guillian Bare Syndrome

Schemes of Pediatrics NMT10

Juevinillie Myasthenia Gravis

Easy Fatigability on repetition of muscular activity improved

o Motor area 4 

Schemes of Pediatrics NMT10

Proximal Muscles . Not Distal

Arch cerebellum connected to Cochlea of the inner ear Drunken Gait

Schemes of Pediatrics NMT10

Emotions & associated Movements ... 

Control ms. Tone according to Neurotransmitters

Mediators of the basal ganglia

Meningitis & Encephalitis Infection

Chronic: X-ray Silver Needle

Craniostenosis Premature closure of sutures

Non Paralytic causes

Physiological delay Lulls Phenomena

Schemes of Pediatrics NMT10

Painful condition: Fracture bones- Arthritis- Scurvy- Dislocation Hip

All above causes are TRANSIENT

All UMNL & LMNL C.P- Hydrocephalus Meningitis

All above causes are PERMENANT

Can be Transient by ttt

Primary Inability to Walk

Secondary Inability to Walk

Schemes of Pediatrics NMT10

Audible sounds: (Noisy respiration)

Upper respiratory system Nose, mouth , nasopharynx & larynx

& 1J $8%

Schemes of Pediatrics NMT10

Protoporphyrin Indirect Billirubin Liver Direct Billirubin Bile

" & ( RBCs Hemolysis"

o Motor area 4

Emotions & associated Movements ...

& 1J $8%

Fine : unhealthy alveolar

Coarse : air passage through

Ronchi #DE C.DE

Sibilant "! :

so the action of k on smooth ms is different of thay on skeletal ms. ( !(