794
د. ماجد محمد المبشر قناه طبيه مفيده💞 مرحبا بكم في قناتي🌹
رساله صباحيه تحمل كل الحب❤️
شكرا لكم من القلب❤️
طلاب جامعه العلوم والتقانه❤️
الدفعه ٢١ لكم مني كل الحب ❤️😍
(JVP)
• Mild edema.
• Oliguria and hematuria.
Aetiology:
Post-streptococcal infection (group A beta hemolytic streptococci)
Upper respiratory tract infection or skin infection latent period (1-3w)
Immune complex formation deposition in glomeruli Glomerulonephritis.
Pathophysiology:
1. Oliguria: due to decreased glomerular permeability & narrowing of the afferent
arteriole.
2. Hematuria: injury of the capillary wall.
3. Hypertension:
• V.C of the afferent arteriole causes increase of renin.
• Na & H2O retention.
4. High JVP: due to hypervolemia (Na&H2O retention).
5. Odema: Na&H2O retention, HF, Toxic capillaritis.
Clinical picture:
1- Acute onset.
2- Young age (usually below 20 ys).
3- History of streptococcal infection (pharyngitis, pyoderma).
4- General ( Fever, Headache, Malaise, Anorexia).
5- Local (loin pain & tenderness)
6- Hypertension (acute onset, never severe but may lead to complications due to
acute onset & young age).
7- Congested neck veins.
8- Mild odema: periorbital then in the face then generalized.
9- Oliguria & Hematuria.
10- Anemia: due to bone marrow depression (immune complex).
Complications:
Complications of hypertension {see cardiology… wait u can see it here ☺}
1-Cardiac :
o LSHF : due to pressure overload .
o Ischemic heart disease : due to atherosclerosis & hypertrophy .
o Bernheim effect : ( signs of RSHF )
Hypertrophy of LV may cause bulging of the septum in th RV
leading to slight impairment of the filling of RV sig
2-Cerebral :
o Cerebral atherosclerosis .
o Cerebral ischemia & thrombosis ( infarction )
o Cerebral hemorrhage ( stroke )
o Hypertensive encephalopathy :
As a result of acute rise of BP , the cerebral blood vessels are no longer
able to maintain the necessary degree of constriction ( failure of auto
regulation ) & they begin to dilate cerebral blood flow ICT , brain
edema , coma & convulsion may occur .
NB : How to differentiate between stroke & hypertensive encephalopathy?
Stroke : Signs of lateralization ( unilateral )
Hypertensive encephalopathy : No signs of lateralization ( bilateral )
3-Renal :
o Renal failure .
o Hematuria & proteinuria .
4-Retinal : 4 grades
o Grade I : Thickening of retinal arterioles ( silver wire appearance ).
o Grade II : Kinking of retinal veins .
o Grade III : Hemorrhage & exudates .
o Grade IV : Papilloedema .
5-Vascular :
o Atherosclerosis .
o Aortic dissection .
Investigations:
Urine Examination Examination
o Volume: oliguria ( less than 400 ml/d)
o Specific gravity: increased
o Casts: red cell casts
o Hematuria (coca cola like): dysmorphic RBC`S
Blood Examina Examination
o Anemia
o Increased ESR
o Leucocytosis
o Urea & creatinine may be elevated
o Increased Na & K
Renal F Renal Function unction unction Tests
o Glomerular: impaired
o Tubular: normal
Renal B Renal Biopsy
Not needed for diagnosis But, in prolonged cases to exclude other diseases.
Investigations for the cause Investigations for the cause
o Increased ASO titre
o Anti-streptokinase
o Culture (swabs from throat)
Prognosis:
Self limited disease in most of patients.
• 90% : complete recovery.
• 5% : rapidly progressive glomerulonephritis leading to renal failure.
• Few patients : develop acute renal failure, hypertensive encephalopathy &heart
failure.
Treatment:
1- Diet:
↓ H2O, Na, K, Protein.
2- Drugs:
• Treatment of HTN and its complications.
• Antibiotics: crystalline penicillin(1 million u/6h iv for 1w).
Cortisone is contraindicated as it increases blood pressure.
Cortisone is indicated only in collagen diseases.
3- Dialysis: Dialysis:
5% leads to Acute renal failure.
اخر شي
DIFFERENTIAL DIAGNOSIS OF HEMATURIA
Pre-Renal: ( systemic causes)
o Hemorrhagic blood disorders:
o Hemorrhagic fever.
o Severe HTN.
o Heparin.
o Angiomatus malformation.
o Aneurysm.
o Tumor.
o Trauma.
Renal:
o Nephritic syndrome
o Tumors ( hypernephroma)
o Stone
o Infection
Primary Sclerosing Cholngitits
PSC results from inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts leading to narrowing throughout the biliary system.
Cause ?
- Unknown, immunological mechanisms have been suggested.
- 70% of patients have inflammatory bowel disease (usually ulcerative colitis).
Clnical Picture
- Asymptomatic.
- Pruritis, jaundice and occasionally abdominal pain.
- Liver cirrhosis and portal hypertension can develop.
Investagtion
- ERCP showing multiple strictures with beading of bile ducts.
- ANCA antibodies are positive in 80% of cases.
Treatment
- It is unsatisfactory.
- Steroids, azathioprine, methotrexate and ursodeoxycholic acid may be
helpful to some patients.
- Biliary strictures can be dilated or stented at endoscopy.
- Liver transplantation should be considered in advanced cases.
بسم الله الرحمن الرحيم
اللهم ارحم دكتور زهير وصبرنا وقوينا يارب
الحمد لله ...فقدنا ابونا ومعلمنا واستاذنا ودكتورنا
واتكسر ضهرنا والله العظيم
قلبي م مطاوعني اني امسك قلم او اكتب أو اشرح شي وأبوي متوفي😭😭 بس دي رسالتو ونحنا حنواصل فيها😭😭
خافو ربكم في مرضاكم
خافو ربكم في قرايتكم
الدنيا نهايتها شبر في شبر
انتو أطباء المستقبل😭😭
خافو ربنا😭
الحمد لله بي قلب منكسر وحزين جدا
بحاول اثبت نفسي وأحاول اشرح شي
ودي الصدقه الجاريه علي روح ابونا
القراها لييينا😭😭
الله يرحمك ويغفر ليك ي ابوي
الليله اللكشر الحنتكلم فيهو عن
Gall bladder & Biliary system
Anatomy of Biliary system :
عارف كلكم عارفين الانتومي
The- right & left- hepatic- duct-
arise- from- the- right- &- left-
lobes- of- the- liver- &- unite-
to- form- the- common-hepatic-
duct- which- is- joined- by- the- cystic- duct- from- the- gall- bladder- to- form- the- common- bile- duct- (- CBD- )-
which- enters- the- duodenum- often- after- joining- the- main- pancreatic-
duct- )- through- the- ampulla- of- vater.-
The- function- of- the- gall- bladder- is- to- store- bile- that- is- produced- in- the- liver- before- the- bile- is- secreted- into- the- intestines
نبدا بسم الله
Gall stones
👍Etiology :
1) Cholesterol stones :
Cholesterol is kept soluble by the presence of bile salts so , if bile salts decrease or cholesterol increases , cholesterol stones will occur.
2) Pigment stones : rare
Excessive production of bile pigments in bile e.g. chronic hemolysis. 80% gallstones are a mixture of cholesterol & bile pigment ( mixed stones )
3) Stasis :
o Estrogen : due to GB wall relaxation.
o Long term parenteral nutrition : lack of oral intake -
cholecystokinin that
stimulate the GB contraction.
👍Risk factors for stone بصformation :
- Fatty ( obesity ) - Forty ( increasing age ) - Fertile ( multi parity ) - Female.
- DM - Drugs : contraceptive pills , Octreotide.
NB : Stones may form in the CBD even after cholecystectomy.
Clinical picture : gall stones are present in 10 - 20% of population
o Asymptomatic : 80% of cases.
o Ascending cholangitis ( bacterial infection )
o Pancreatitis. o Biliary colic.
o Cholecystitis.
o Obstructive jaundice if duct obstruction.
Investigations :
o US : should be performed routinely in patients suspected of having gallstone disease
o ERCP : best one
NB : The- major- component- of- most- gallstones- is- cholesterol,- which- is- not- radio opaque.-
This- explains- why- many- gallstones-do- not- show- up- n- a- plain- X ray;only- stones- with- high- calcium- content-
are-radio opaque- and- visible
Treatment :
o Cholecystectomy is a definitive treatment (-
either- surgical-
or- by- laparoscope-
o Shock wave lithotripsy.
o Medical treatment : through the oral administration of bile acids, such as ursodeoxycholic acid to dissolve cholesterol stones
بس ده المهم عندكم
بعد ده نمش لي
Acute cholecystitis
Etiology & pathophysiology :
o It’s usually caused by obstruction of the cystic duct by stones.
o Begins with sterile inflammation , then becomes infected ( E.coli , Strept. fecalis )
o GB may distended with mucous (catarrhal cholecystitis) or pus ( suppurative cholecystitis ) .
o Rarely, acute gangrenous cholecystitis may develop.
Symptoms : Severe pain
وين ختتو وبمش وين؟
في
RUQ or In epigatric area
Radiated into back or right shoulder
o Nausea & vomiting may occur.
Signs :
o Fever.
o Obstructive jaundice may occur due to edema or stone in CBD.
o Murphy’s sign : ask the patient to take deep inspiration while palpating the G.B.
area -
the patient catch his breath due to sudden pain.
o Boas’s sign : there is an area of hyperesthesia between the 9th and 11th ribs
posteriorly on the right side.
Investigations :
1- Laboratory :
o Leucocytosis.
o Serum bilirubin , AST , ALT & alkaline phosphates : may be elevated.
2- Radiological : US , Radioisotope scanning.
3- ECG : done as a routine especially in the elderly patients to exclude IHD.
Treatment :
Medical :
o Bed rest , IV fluid.
o Analgesics : pet
سافر بأحلامك الوردية إلى دروب المستحيل لا تخف فقط ثق بإمكانياتك التي ستصنعك في يوم ما، لا تبالي بجراح يديك ستطيب مع الوقت الأهم الآن أمانيك 💛💫
تصبحون على خير 🌼
( pyelonephritis)
Post RenaL
o Trauma ( catheter)
o Stone bladder
o Tumor bladder
o Infection ( cystitis)
N.B The most common cause of hematuria is UTI
Differential diagnosis of polyuria
1. Physiological :
Winter months.
Excess coffee or tea.
Diuretics.
2. Psychological : Hysterical polydepsia.
3. Pathological :
a. Endocrinal :
i. D.I.
ii. D.M.
iii. Adrenal : Conn’s , Cushing’s , Addison’s.
iv. Thyroid : thyrotoxicosis.
v. Parathyroid : hyperparathyroidism.
b. Renal :
i. Nephrogenic DI .
ii. Chronic renal failure
iii. Diuretic phase of acute renal failure.
c. After any attack :
i. Migraine
ii. Epilepsy
iii. Bronchial asthma
iv. PSVT
اللكشر التاني
في الرينل باثولجي
NEPHROTIC SYNDROME
👍Definition:
Syndrome characterized by :
1. Heavy proteinuria (more than 3.5 gm/d)
2. Hypoprotinemia (albumin is less than2.5 gm/dl)
3. Generalized edema.
4. Dyslipidemia (elevated cholesterol,TG,......)
Aetiology:
Primary (80%)
• Minimal change Glomerulonephritis (GN) : in children
• Membranous GN : in adult
• Membranoproliferative GN
• Mesingoproliferative GN
Secondary
• Infection: HBV, Malaria, T.B
• Immune: SLE, PAN
• Metabolic: DM, Amyloidosis
• Malignancy: Lymphoma, M.myeloma
• Vascular: HF, Renal vein thrombosis
• Drugs: Penicillamine, Gold, NSAIDs
Pathophysiology
• Heavy protenuria: due to increased the glomerular permeability.
o Selective proteinuria: good prognosis
o Non selective proteinuria: bad prognosis
• Hypoproteinemia: due to proteinuria, GIT edema leading to malabsorption
• Oedema: due to hypoproteinemia, hyperaldosteronism, increased ADH,
decreased sensitivity to ANP.
• Dyslipidemia: increased hepatic synthesis stimulated by decreased albumin
leading to increased albumin & lipoprotein.
• Na: the total Na is increased due to increased aldosterone But, Na may decreased
in blood (escape with edema).
• K: decreased due to increased aldosterone, diuretics, and steroids.
• Ca: decreased bound Ca due to decreased albumin.
free Ca is normal &maybe decreased.
Clinical picture
Oedema
• Generalized.
• Gradual onset.
• Pitting.
• Puffiness (start periorbital then face then sacrum then genitalia then general)
• Associated with serous effusion.
Hypoproteinemia
• Muscle wasting
• Osteoprosis
• Decreased transferrine leading to anemia
• Loss of immunoglobulins in urine leading to recurrent infection
• Loss of thyroxin binding protein leading to hypothyrodism
• Increased toxicity of drugs
Hypokalemia
• Muscle weakness & paralysis
• Arrhythmia & ECG changes
• Hypokalemic nephropathy
Hypercoagulability
• Due to hypovolemia, loss of antithrombin 3
• DVT leading to PE (sudden death)
• Renal vein thrombosis
No tetany.
• Decreased bound Ca only
• Free Ca is still normal in most cases
No oliguria.
• Tubular function is normal
No hematuria.
No hypertension .
Causes of hypertension in Nephrotic syndrome
Nephritic nephrotic.
Collagen diseases.
D.M
Steroid.
Differential Diagnosis:
o DD of generalized edema : see later
o DD of proteinuria : see later
Investigations
Urine examination: Urine examination:
• Volume: Normal
• Specific gravity: Normal
• Casts: Hyaline & Lipid casts
• Proteinuria: more than 3.5 gm/d
Blood examination: Blood examination:
• Increased ESR
• Increased cholesterol, TG, LDH, VLDL
• Anemia
• Decreased Na ,K, Ca
Total Na is increased But, Na in blood may be decreased (escape with edema)
Renal function tests: Renal function tests:
• Normal
Renal biopsy: Renal biopsy:
Indications:
• Hypertension.
• Hematuria.
Not indicated in children since diagnosis is minimal change GN
Investigations for the cause: Investigations for the cause:
e.g:
ANA for collagen diseases
Blood glucose
Treatment
Diet:
H2O: it is better to keep the patient in slight –ve balance
Na: decreased
K: increased
Protein: increased (to compensate the loss)
Drugs:
Oedema
o Lasix : it may lead to hypovolemia & ARF
o Spironolactone : to decrease aldosterone.
Hypoproteinemia
o High protein
o ACEIs : decrease proteinuria
o Antibiotic : for recurrent infections
Hypokalemia
o Potassium
Hypercoagulability
o Oral anticoagulant
o Heparin is not used because it acts through anithrombin 3 which is lost in
urine
Salt free albumin
o In resistant cases
Cortisone (60 mg/d for 1m then 30 mg/d for 2m)
Immunosuppressive
o Cyclophosphamide
o Azathioprine
Dialysis:
Patient passing to renal failure.
طيب وعشان تفهمو الفرق بينا وبين
NEPHRITIC SYNDROME
Definition:
Syndrome characterized by acute onset of :
• Hypertension.
• High jugular venous pressure
hidine ( no morphine as it induces spasm of the sphincter of Oddi )
o Antibiotic : 3rd generation cephalosporin. o Antiemetic.
Surgical :
o If the attack subsides , cholesystectomy is done after 1- 3 months.
o Urgent surgery : in cases with complications.
طيب نمش لي اهم تالت شي
Chronic Calculus Cholecystitis
Etiology : It’s almost always associated with the presence of gall stones.
Clinical picture :
o There are recurrent attacks of right upper abdominal pain.
o Dyspepsia , local tenderness & Murphy’s sign is usually present.
Investigations : US shows thick G.B. wall & gall stones.
Treatment : Cholecystectomy.
-
Acetaminophen Posing In children
By Dr.majid Almubasher
لاتنسو الدعاء لدكتور زهير😭😭
اللهم ارحمه واغفر له وثبته عن السؤال
هذه صدقه جارية لي روحو😭😭
حاشتغل كل يوم لكشر كامل صدقه جاريه ليه😭😭😭😭
الحمد لله علي كل حال😭😭