•What are the signs of active acromegaly?
-Signs of activity:
1-Progressive increase in the size of the body
2-Excessive sweating
3-Increasing visual field defect
4-Large skin tags (Molluscum fibrosum)
5-Presence of glycosuria (diabetes mellitus)
6-Hypertension
7-Progressive headache
8-Enlarging thyroid.
#MCQ
#Medicine
#Endocrine
-Signs of activity:
1-Progressive increase in the size of the body
2-Excessive sweating
3-Increasing visual field defect
4-Large skin tags (Molluscum fibrosum)
5-Presence of glycosuria (diabetes mellitus)
6-Hypertension
7-Progressive headache
8-Enlarging thyroid.
#MCQ
#Medicine
#Endocrine
In case of Cushing syndrome:
-CBC shows
1-High Neutrophils & RBC, but decrease all other cells (Lymphopenia, Esinopenia).
-Biochemistry shows:
1-Hyperglycemia
2-Hypernatremia.
3-Hypokalemia.
4-Metabolic alkalosis
5-Hypocalcemia.
#Medicine
#Endocrine
-CBC shows
1-High Neutrophils & RBC, but decrease all other cells (Lymphopenia, Esinopenia).
-Biochemistry shows:
1-Hyperglycemia
2-Hypernatremia.
3-Hypokalemia.
4-Metabolic alkalosis
5-Hypocalcemia.
#Medicine
#Endocrine
•In case of Primary Adrenal insufficiency"Addison's disease ":
-CBC: neutropenia, lymphocytosis and eosinophilia.
-Decrease Aldosterone,
-Hyponatremia,
-Hyperkalemia,
-Metabolic acidosis.
-Hypercalcemia.
-Hypoglycemia.
Urea is increased in primary disease but decreased or Normal in secondary diseas.
#Medicine
#Endocrine
-CBC: neutropenia, lymphocytosis and eosinophilia.
-Decrease Aldosterone,
-Hyponatremia,
-Hyperkalemia,
-Metabolic acidosis.
-Hypercalcemia.
-Hypoglycemia.
Urea is increased in primary disease but decreased or Normal in secondary diseas.
#Medicine
#Endocrine
•Causes of anaemia in malaria infection:
1-Haemolysis of infected red cells
2-Haemolysis of non-infected red cells(black water fever) 3-Dyserythropoiesis
4-Splenomegaly and sequestration
5-Folate depletion.
#Medicine
#Infections
1-Haemolysis of infected red cells
2-Haemolysis of non-infected red cells(black water fever) 3-Dyserythropoiesis
4-Splenomegaly and sequestration
5-Folate depletion.
#Medicine
#Infections
•What is AIDS?
-It is HIV infected individual with CD4 T cell count <200 cells/mm2 regardless of the presence of the symptoms.
or
-HIV infected individual with AIDS defining conditions (category C) regardless of CD4 count is labeled AIDS.
#Medicine
#Infection
-It is HIV infected individual with CD4 T cell count <200 cells/mm2 regardless of the presence of the symptoms.
or
-HIV infected individual with AIDS defining conditions (category C) regardless of CD4 count is labeled AIDS.
#Medicine
#Infection
•HIV disease:
-It is the spectrum of disorders ranging from primary infection, with or without the acute HIV syndrome, to the asymptomatic infected state to advanced disease.
#Medicine
#Infection
-It is the spectrum of disorders ranging from primary infection, with or without the acute HIV syndrome, to the asymptomatic infected state to advanced disease.
#Medicine
#Infection
•What are the commonest causes of PUO?
-Tuberculosis, collagen disease (e.g. SLE), malignancy (e.g. lymphoma, renal cell carcinoma).
#Medicine
#Infection
-Tuberculosis, collagen disease (e.g. SLE), malignancy (e.g. lymphoma, renal cell carcinoma).
#Medicine
#Infection
•What are the causes of good appetite
but loss of weight?
1-Diabetes mellitus.
2-Thyrotoxicosis.
3-Kala-azar.
4-Sometimes in malabsorption syndrome.
#Medicine
#Metabolic
but loss of weight?
1-Diabetes mellitus.
2-Thyrotoxicosis.
3-Kala-azar.
4-Sometimes in malabsorption syndrome.
#Medicine
#Metabolic
•What are the mechanisms of anemia in kala-azar?
1-Hypersplenism (which causes sequestration and splenic pooling, destruction of RBC in spleen).
2-Short lifespan of RBC
3-Hemolysis
4-Ineffective erythropoiesis ,infiltration of marrow by parasite
5-Bleeding, hemodilution.
#Medicine
#Infection
1-Hypersplenism (which causes sequestration and splenic pooling, destruction of RBC in spleen).
2-Short lifespan of RBC
3-Hemolysis
4-Ineffective erythropoiesis ,infiltration of marrow by parasite
5-Bleeding, hemodilution.
#Medicine
#Infection
•What are the causes of anemia in CKD?
-Anemia is common in CKD, correlates with the severity of renal failure.
-It is usually normocytic and normochromic.
-The mechanisms are:
1-Erythropoietin deficiency (most significant)
2-Diminished erythropoiesis due to toxic effects of uremia on bone marrow suppression. Also by PTH, ACE inhibitor
3-Reduced dietary intake and absorption of hematinics (iron, vitamin B12, folic acid).
4-Increased red cell destruction (may also be during hemodialysis due to mechanical, oxidant and thermal damage)
5-Increased blood loss due to capillary fragility, poor platelet function, occult gastrointestinal bleeding and blood loss during hemodialysis.
6-Erythropoietin alpha therapy may cause anemia (by pure red cell aplasia).
#Medicine
#Renal
-Anemia is common in CKD, correlates with the severity of renal failure.
-It is usually normocytic and normochromic.
-The mechanisms are:
1-Erythropoietin deficiency (most significant)
2-Diminished erythropoiesis due to toxic effects of uremia on bone marrow suppression. Also by PTH, ACE inhibitor
3-Reduced dietary intake and absorption of hematinics (iron, vitamin B12, folic acid).
4-Increased red cell destruction (may also be during hemodialysis due to mechanical, oxidant and thermal damage)
5-Increased blood loss due to capillary fragility, poor platelet function, occult gastrointestinal bleeding and blood loss during hemodialysis.
6-Erythropoietin alpha therapy may cause anemia (by pure red cell aplasia).
#Medicine
#Renal
Causes of an extremely elevated Erythrocyte Sedimentation rate (>100 mm/h):
•Infectious diseases (35–40٪):
1-Subacute bacterial endocarditis
2-Abscesses
3-Osteomyelitis
4-Tuberculosis
5-Urinary tract infection.
•Inflammatory diseases (15–20)
1-Giant cell arteritis
2-Rheumatoid arthritis
3-SLE.
•Malignancies (15–20):
1-Multiple myeloma
2-Leukemias
3-Lymphomas
4-Carcinomas.
•Other (20–35):
1-Drug hypersensitivity reactions (drug fever)
2-Ischemic tissue injury/trauma
3-Renal diseases.
#Infections
•Infectious diseases (35–40٪):
1-Subacute bacterial endocarditis
2-Abscesses
3-Osteomyelitis
4-Tuberculosis
5-Urinary tract infection.
•Inflammatory diseases (15–20)
1-Giant cell arteritis
2-Rheumatoid arthritis
3-SLE.
•Malignancies (15–20):
1-Multiple myeloma
2-Leukemias
3-Lymphomas
4-Carcinomas.
•Other (20–35):
1-Drug hypersensitivity reactions (drug fever)
2-Ischemic tissue injury/trauma
3-Renal diseases.
#Infections
In HIV&AIDS:
About Vaccines.
-All patients should be given a conjugate pneumococcal vaccine and annual influenza vaccination. Hepatitis B vaccination should be given to those who are not immune.
-In the UK, the following additional vaccines are also recommended:
• hepatitis A: in those at risk
• human papillomavirus: in people <
40 years old
• measles, mumps and rubella (MMR): in those with negative measles serology
• meningococcus: in people < 25 years old, those with asplenia or complement deficiency, during outbreaks
• diphtheria/tetanus/acellular pertussis (dTaP)/inactivated poliovirus vaccine (IPV): meeting general indications
• chickenpox: if seronegative; those who are seropositive should receive the shingles vaccine.
Bacille Calmette–Guérin (BCG) is contraindicated in all HIV-infected people.
#Infections
About Vaccines.
-All patients should be given a conjugate pneumococcal vaccine and annual influenza vaccination. Hepatitis B vaccination should be given to those who are not immune.
-In the UK, the following additional vaccines are also recommended:
• hepatitis A: in those at risk
• human papillomavirus: in people <
40 years old
• measles, mumps and rubella (MMR): in those with negative measles serology
• meningococcus: in people < 25 years old, those with asplenia or complement deficiency, during outbreaks
• diphtheria/tetanus/acellular pertussis (dTaP)/inactivated poliovirus vaccine (IPV): meeting general indications
• chickenpox: if seronegative; those who are seropositive should receive the shingles vaccine.
Bacille Calmette–Guérin (BCG) is contraindicated in all HIV-infected people.
#Infections
Conditions required for safe percutaneous liver biopsy:
• Cooperative patient
• Prothrombin time < 4 secs prolonged
• Platelet count > 80 × 109/L
• Exclusion of bile duct obstruction, localised skin infection, advanced chronic obstructive pulmonary disease, marked ascites and severe anaemia.
#Liver
• Cooperative patient
• Prothrombin time < 4 secs prolonged
• Platelet count > 80 × 109/L
• Exclusion of bile duct obstruction, localised skin infection, advanced chronic obstructive pulmonary disease, marked ascites and severe anaemia.
#Liver
•What are the causes of fluctuating jaundice?
1-Choledocholithiasis
2-Choledochal cyst
3-Sometimes in primary sclerosing cholangitis
4-Hemolytic jaundice
5-Wilson disease
6-Gilbert’s syndrome
7-Benign recurrent intrahepatic cholestasis (BRIC)
8-Recurrent pancreatitis.
#Liver
1-Choledocholithiasis
2-Choledochal cyst
3-Sometimes in primary sclerosing cholangitis
4-Hemolytic jaundice
5-Wilson disease
6-Gilbert’s syndrome
7-Benign recurrent intrahepatic cholestasis (BRIC)
8-Recurrent pancreatitis.
#Liver
•What are the causes of progressive jaundice?
1-Carcinoma of the head of the pancreas
2-Cholangiocarcinoma
3-Primary biliary cirrhosis
4-Primary sclerosing cholangitis.
#Liver
1-Carcinoma of the head of the pancreas
2-Cholangiocarcinoma
3-Primary biliary cirrhosis
4-Primary sclerosing cholangitis.
#Liver
•What are the intrahepatic causes of cholestatic (obstructive) jaundice
1-Primary biliary cirrhosis
2-Primary sclerosing cholangitis
3-Viral hepatitis (especially HEV)
4-Drugs and alcohol
5-Autoimmune hepatitis
6-Cystic fibrosis
7-Postoperative
8-Benign recurrent intrahepatic cholestasis
9-Pregnancy.
#Liver
1-Primary biliary cirrhosis
2-Primary sclerosing cholangitis
3-Viral hepatitis (especially HEV)
4-Drugs and alcohol
5-Autoimmune hepatitis
6-Cystic fibrosis
7-Postoperative
8-Benign recurrent intrahepatic cholestasis
9-Pregnancy.
#Liver
•What are the congenital nonhemolytic hyperbilirubinemia?
1.Gilbert’s syndrome (unconjugated hyperbilirubinemia)
2.Crigler-Najjar syndrome (unconjugated hyperbilirubinemia)
3. Dubin-Johnson syndrome (conjugated hyperbilirubinaemia)
4. Rotor’s syndrome (conjugated hyperbilirubinemia).
#Liver
1.Gilbert’s syndrome (unconjugated hyperbilirubinemia)
2.Crigler-Najjar syndrome (unconjugated hyperbilirubinemia)
3. Dubin-Johnson syndrome (conjugated hyperbilirubinaemia)
4. Rotor’s syndrome (conjugated hyperbilirubinemia).
#Liver
Gilbert’s syndrome:
-It is inherited as autosomal dominant.
-There is reduction of glucuronyl transferase and abnormality in uptake of bilirubin.
-Mild jaundice, especially with fasting.
-No treatment is necessary, only reassurance is sufficient.
#Liver
-It is inherited as autosomal dominant.
-There is reduction of glucuronyl transferase and abnormality in uptake of bilirubin.
-Mild jaundice, especially with fasting.
-No treatment is necessary, only reassurance is sufficient.
#Liver
Crigler-Najjar syndrome:
There are two types:
•Type I is inherited as autosomal recessive.
-There is absence of glucuronyl transferase, the patient dies in neonatal period due to kernicterus.
•Type II is inherited as autosomal dominant.
-There is reduction of glucuronyl transferase.
-The patient usually survives up to adulthood.
-Treatment is by phenobarbitone, ultraviolet light or liver transplantation.
#Liver
There are two types:
•Type I is inherited as autosomal recessive.
-There is absence of glucuronyl transferase, the patient dies in neonatal period due to kernicterus.
•Type II is inherited as autosomal dominant.
-There is reduction of glucuronyl transferase.
-The patient usually survives up to adulthood.
-Treatment is by phenobarbitone, ultraviolet light or liver transplantation.
#Liver
Rotor’s syndrome:
- It is inherited as autosomal recessive.
-There is defect in uptake and conjugation bilirubin in the liver.
-Mild disease.
-Urinary total coproporphyrin is increased.
-No treatment is necessary.
#Liver
- It is inherited as autosomal recessive.
-There is defect in uptake and conjugation bilirubin in the liver.
-Mild disease.
-Urinary total coproporphyrin is increased.
-No treatment is necessary.
#Liver
Dubin-Johnson syndrome:
- It is inherited as autosomal recessive.
-There is defect in excretion of bilirubin.
-Usually mild disease.
-Liver is black due to deposition of lipofuscin and melanin.
-Urinary coproporphyrin I is increased.
-No treatment is necessary.
#Liver
- It is inherited as autosomal recessive.
-There is defect in excretion of bilirubin.
-Usually mild disease.
-Liver is black due to deposition of lipofuscin and melanin.
-Urinary coproporphyrin I is increased.
-No treatment is necessary.
#Liver