#Clinical_case 28
A 47-year-old woman presents to the emergency room complaining of a 4-week history of progressive abdominal swelling and discomfort. She has no other gastrointestinal symptoms, and she has a normal appetite and normal bowel habits. She is married for 20 years.
PMH π excessive blood loss in previous pregnancy, which required a blood transfusion
D.H π Negative
H.H π No smoking/ drinks occassionally/ Snored cocaine once or twice many years ago
π Physical examination:
Head and neck π Sclerae are icteric
Chest π Symmetric/ Clear to auscultation
Abdomen π Swollen with mild diffuse tenderness/ distented/ Shifting dullness to percussion and a fluid wave/ Hypoactive bowel sounds
Extremities π Normal
π Vital signs:
BP = 94/60 mmHg
PR = 88 bpm
RR = 18/min
T = 38Β°C
π Laboratory results:
Na = 129 mEq/L
Alb = 2.8 mg/dL
Total bilirubin = 4mg/dL
PTT = 15 sec
INR = 1
WBC = 5,600
Hgb = 12 g/dL
MCV = 102 fL
Plt = 78,000
ββββββββββ
1β£ Differential diagnosis?
2β£ Most likely diagnosis?
3β£ Next step?
A 47-year-old woman presents to the emergency room complaining of a 4-week history of progressive abdominal swelling and discomfort. She has no other gastrointestinal symptoms, and she has a normal appetite and normal bowel habits. She is married for 20 years.
PMH π excessive blood loss in previous pregnancy, which required a blood transfusion
D.H π Negative
H.H π No smoking/ drinks occassionally/ Snored cocaine once or twice many years ago
π Physical examination:
Head and neck π Sclerae are icteric
Chest π Symmetric/ Clear to auscultation
Abdomen π Swollen with mild diffuse tenderness/ distented/ Shifting dullness to percussion and a fluid wave/ Hypoactive bowel sounds
Extremities π Normal
π Vital signs:
BP = 94/60 mmHg
PR = 88 bpm
RR = 18/min
T = 38Β°C
π Laboratory results:
Na = 129 mEq/L
Alb = 2.8 mg/dL
Total bilirubin = 4mg/dL
PTT = 15 sec
INR = 1
WBC = 5,600
Hgb = 12 g/dL
MCV = 102 fL
Plt = 78,000
ββββββββββ
1β£ Differential diagnosis?
2β£ Most likely diagnosis?
3β£ Next step?
β€2
#Clinical_case_answer 28
1β£ Differential diagnosis:
1) High grade fatty liver disease
2) Cirrhosis
3) Hepatocellular carcinoma
4) Hepatitis
5) Hemochromatosis
6) Wilson's disease
2β£ Most likely diagnosis:
π "Hepatic cirrhosis"
Clinical approach:
Cirrhosis is the end result of chronic hepatocellular injury that leads to both fibrosis and nodular regeneration. With ongoing hepatocyte destruction and collagen deposition, the liver shrinks in size and becomes nodular and hard. Alcoholic cirrhosis is one of the most common forms of cirrhosis. It is related to chronic alcohol use, but there appears to be some hereditary predisposition to the development of fibrosis, and the process is enhanced by concomitant infection with hepatitis C. Clinical symptoms are produced by the hepatic dysfunction as well as by portal hypertension, which is produced by increased resistance to portal blood flow, producing portal hypertension, and sometimes to resultant portosystemic shunting. Loss of functioning hepatic mass leads to jaundice as well as impaired synthesis of albumin (leading to edema) and of clotting factors (leading to coagulopathy). Fibrosis and increased sinusoidal resistance lead to portal hypertension and its complications, such as esophageal varices, ascites, and hypersplenism. Portosystemic shunting via natural collaterals or iatrogenic shunts causes hepatic encephalopathy. Portal hypertension causes caput medusa and hemorrhoids. Decreased liver production of steroid hormone binding globulin (SHBG) leads to an increase in unbound estrogen manifested by spider angioma, palmar erythema and gynecomastia
3β£ Next step:
Paracentesis of ascitic fluid (to determine its likely etiology as well as evaluate for the complication of SBP)
ββββββββββ
β Final diagnosis:
#Cirrhosis probably hepatitis C-related
1β£ Differential diagnosis:
1) High grade fatty liver disease
2) Cirrhosis
3) Hepatocellular carcinoma
4) Hepatitis
5) Hemochromatosis
6) Wilson's disease
2β£ Most likely diagnosis:
π "Hepatic cirrhosis"
Clinical approach:
Cirrhosis is the end result of chronic hepatocellular injury that leads to both fibrosis and nodular regeneration. With ongoing hepatocyte destruction and collagen deposition, the liver shrinks in size and becomes nodular and hard. Alcoholic cirrhosis is one of the most common forms of cirrhosis. It is related to chronic alcohol use, but there appears to be some hereditary predisposition to the development of fibrosis, and the process is enhanced by concomitant infection with hepatitis C. Clinical symptoms are produced by the hepatic dysfunction as well as by portal hypertension, which is produced by increased resistance to portal blood flow, producing portal hypertension, and sometimes to resultant portosystemic shunting. Loss of functioning hepatic mass leads to jaundice as well as impaired synthesis of albumin (leading to edema) and of clotting factors (leading to coagulopathy). Fibrosis and increased sinusoidal resistance lead to portal hypertension and its complications, such as esophageal varices, ascites, and hypersplenism. Portosystemic shunting via natural collaterals or iatrogenic shunts causes hepatic encephalopathy. Portal hypertension causes caput medusa and hemorrhoids. Decreased liver production of steroid hormone binding globulin (SHBG) leads to an increase in unbound estrogen manifested by spider angioma, palmar erythema and gynecomastia
3β£ Next step:
Paracentesis of ascitic fluid (to determine its likely etiology as well as evaluate for the complication of SBP)
ββββββββββ
β Final diagnosis:
#Cirrhosis probably hepatitis C-related
π5β€1
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Paracentesis
Paracentesis
#Clinical_case 29
An 8-year old girl has been brought to the hospital with a complaint of generalized skin manifestations. The young girl was taken to a local clinic on an outpatient basis about 10 days ago following a sore throat and fever.
The physician diagnosed her with a cold and started Amoxicillin for her. 3 days after start taking amoxicillin, she developed skin rashes that started on the head and face that spread to the chest and abdomen after a few hours that was accompanied by lip swelling and dyspnea. Following a quick visit to a hospital, hydrocortisone and clindamycin was prescribed for her.
During hospitalization, swelling of the lips and dyspnea improved, but skin rashes spread to the back and buttocks.
π Physical examinations:
Neck π Small 1*1cm lymph node on the lateral side of the neck
Pharynx π Erythema and brief hypertrophy of the tonsils without exudate
Skin π
Palpable purpura, generalized on the skin that faded with pressure but doesnt disappeared completely.
(See the pictures below)
ββββββββββ
1β£ Differential diagnosis?
2β£ Required laboratory tests?
3β£ Management?
An 8-year old girl has been brought to the hospital with a complaint of generalized skin manifestations. The young girl was taken to a local clinic on an outpatient basis about 10 days ago following a sore throat and fever.
The physician diagnosed her with a cold and started Amoxicillin for her. 3 days after start taking amoxicillin, she developed skin rashes that started on the head and face that spread to the chest and abdomen after a few hours that was accompanied by lip swelling and dyspnea. Following a quick visit to a hospital, hydrocortisone and clindamycin was prescribed for her.
During hospitalization, swelling of the lips and dyspnea improved, but skin rashes spread to the back and buttocks.
π Physical examinations:
Neck π Small 1*1cm lymph node on the lateral side of the neck
Pharynx π Erythema and brief hypertrophy of the tonsils without exudate
Skin π
Palpable purpura, generalized on the skin that faded with pressure but doesnt disappeared completely.
(See the pictures below)
ββββββββββ
1β£ Differential diagnosis?
2β£ Required laboratory tests?
3β£ Management?
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π Pleural tapping
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Management of GI Bleeding
π Check ABC
π Cardiac monitoring and P.O
π Oxygen supplement therapy
π Lab tests
π Serial ECG
π IV fluid therapy
π Monitoring Hgb level
π NGtube placement
π Blood transfusion
π Proton pump inhibitors
π Prokinetics
π Octreotide
π Band ligation
π Antibiotic
π Surgical consultation
β Watch the video below fully explained
ππππππππ
π Check ABC
π Cardiac monitoring and P.O
π Oxygen supplement therapy
π Lab tests
π Serial ECG
π IV fluid therapy
π Monitoring Hgb level
π NGtube placement
π Blood transfusion
π Proton pump inhibitors
π Prokinetics
π Octreotide
π Band ligation
π Antibiotic
π Surgical consultation
β Watch the video below fully explained
ππππππππ
π9π2