Clinical Simulator π©ββπ§ββ pinned Β«ππππ Hello friends! π Clinical simulator team has started it's activity on youtube! We will share medical videos on our channel which can be used for these purposes: π Your patient's education π Overview of common diseases π Newest methods of treatmentsβ¦Β»
#Clinical_case 26
A 36-year old man has came to the office complaining of some red, painful and fluid-filled lesions on his right arm which has started from 5 days ago. The pain is getting worse over time passing. Today some new lesions have appeared around his right eye which is itchy and painful. He notices no more complaints.
PMH π Negative
D.H π Negative
Physical examinations:
There are some red blisters on lateral part of his right arm and also his right eye which is tender in touch.
Neurological examinations of both eyes are intact.
π Vital signs π Normal
ββββββββββ
1β£ What is the most likely diagnosis?
2β£ What else do you need to know about his history?
3β£ Management?
4β£ What would you tell your patient as part of "patient education"?
A 36-year old man has came to the office complaining of some red, painful and fluid-filled lesions on his right arm which has started from 5 days ago. The pain is getting worse over time passing. Today some new lesions have appeared around his right eye which is itchy and painful. He notices no more complaints.
PMH π Negative
D.H π Negative
Physical examinations:
There are some red blisters on lateral part of his right arm and also his right eye which is tender in touch.
Neurological examinations of both eyes are intact.
π Vital signs π Normal
ββββββββββ
1β£ What is the most likely diagnosis?
2β£ What else do you need to know about his history?
3β£ Management?
4β£ What would you tell your patient as part of "patient education"?
π3
Clinical Simulator π©ββπ§ββ pinned Β«https://youtu.be/1DZ6I4a05moΒ»
#Clinical_case 27
A 54 year old man presents to your office complaining of chronic fatigue and feeling of tireness that has been started since 2 months ago. He also complains of abdominal pain especially in the epigaster and RUQ that happens sometimes, with nausea and decreased appetite. He has last weight for about 5Kg over recent 2 months.
π PMH:
1) DM2 (from 12 years ago)
2) Hypercholesterolemia
π D.H:
1) Metformin 1000mg daily
2) Rosuvastatin 20mg daily
Physical examination:
Head and neck π Both sclera are a bit icterous
Skin π Normal color and turgor
Chest π Normal
Abdomen π No tender/ No distention
Extremities π Normal
ββββββββββ
1β£ Differential diagnosis?
2β£ Most likely diagnosis?
3β£ Management?
A 54 year old man presents to your office complaining of chronic fatigue and feeling of tireness that has been started since 2 months ago. He also complains of abdominal pain especially in the epigaster and RUQ that happens sometimes, with nausea and decreased appetite. He has last weight for about 5Kg over recent 2 months.
π PMH:
1) DM2 (from 12 years ago)
2) Hypercholesterolemia
π D.H:
1) Metformin 1000mg daily
2) Rosuvastatin 20mg daily
Physical examination:
Head and neck π Both sclera are a bit icterous
Skin π Normal color and turgor
Chest π Normal
Abdomen π No tender/ No distention
Extremities π Normal
ββββββββββ
1β£ Differential diagnosis?
2β£ Most likely diagnosis?
3β£ Management?
β€1π1
#Clinical_case_answer 27
1β£ Differential diagnosis:
1) Nonalcoholic fatty liver disease (NAFLD)
2) Hepatocellular carcinoma
3) Hepatitis C
4) Pancreatic cancer
5) Choledocholithiasis
6) Starvation
7) Wilson disease
8) Liver cirrhosis
9) Abetalipoproteinemia
10) Cholangiocarcinoma
2β£ Most likely diagnosis:
According to patient's age, long history of diabetes, decreased energy and appetite and vague abdominal pain, fatty liver can be suspected.
But weight loss of 5Kg and conjunctival jaundice, raise our suspicion of hepatic cancers.
3β£ Management:
πΉDiagnosis of liver cancers as well as fatty liver disease is made by considering the patient's history and examinations, laboratory and paraclinical procedures.
The following tests should be requested in this patient:
π CBC diff
π PT, PTT, INR, Albumin
π AST, ALT, ALP, Bili (T & D)
π LDL, HDL, cholesterol & triglyceride
π Amylase, Lipase
π FBS
π Anti HCVAb
π HBsAg, HBcAg
π Plasma Iron, ferritin and TIBC
π Gamma glutamyl transferase
π Abdominal Ultrasound
ββββββββββ
π The definitive method for diagnosing in these patients is biopsy.
The patient eventually underwent a biopsy. The final diagnosis was high-grade fatty liver disease with no clue of cancer. The patient lost weight in the context of severe loss of appetite from two months ago.
In patients with fatty liver disease and risk factors such as weight loss and jaundice, complete hepatitis diagnostic tests should be performed and the following recommendations are essential:
1) Recommended to lose weight in obese patients
2) Avoid alcohol
3) Regular control of blood sugar under the supervision of a physician
4) Regular exercise program, at least 30 minutes daily
The main treatment in these patients lifystyle change, but in some references, some medications have been recommended, such as:
πVitamin E
πPioglitazone
In advanced cases, Liraglutide can be used to prevent liver fibrosis.
In case of impaired liver enzymes, the liver profile should be checked every three to six weeks until it becomes normal.
ββββββββββ
β Final diagnosis:
#High_grade_fatty_liver_disease
1β£ Differential diagnosis:
1) Nonalcoholic fatty liver disease (NAFLD)
2) Hepatocellular carcinoma
3) Hepatitis C
4) Pancreatic cancer
5) Choledocholithiasis
6) Starvation
7) Wilson disease
8) Liver cirrhosis
9) Abetalipoproteinemia
10) Cholangiocarcinoma
2β£ Most likely diagnosis:
According to patient's age, long history of diabetes, decreased energy and appetite and vague abdominal pain, fatty liver can be suspected.
But weight loss of 5Kg and conjunctival jaundice, raise our suspicion of hepatic cancers.
3β£ Management:
πΉDiagnosis of liver cancers as well as fatty liver disease is made by considering the patient's history and examinations, laboratory and paraclinical procedures.
The following tests should be requested in this patient:
π CBC diff
π PT, PTT, INR, Albumin
π AST, ALT, ALP, Bili (T & D)
π LDL, HDL, cholesterol & triglyceride
π Amylase, Lipase
π FBS
π Anti HCVAb
π HBsAg, HBcAg
π Plasma Iron, ferritin and TIBC
π Gamma glutamyl transferase
π Abdominal Ultrasound
ββββββββββ
π The definitive method for diagnosing in these patients is biopsy.
The patient eventually underwent a biopsy. The final diagnosis was high-grade fatty liver disease with no clue of cancer. The patient lost weight in the context of severe loss of appetite from two months ago.
In patients with fatty liver disease and risk factors such as weight loss and jaundice, complete hepatitis diagnostic tests should be performed and the following recommendations are essential:
1) Recommended to lose weight in obese patients
2) Avoid alcohol
3) Regular control of blood sugar under the supervision of a physician
4) Regular exercise program, at least 30 minutes daily
The main treatment in these patients lifystyle change, but in some references, some medications have been recommended, such as:
πVitamin E
πPioglitazone
In advanced cases, Liraglutide can be used to prevent liver fibrosis.
In case of impaired liver enzymes, the liver profile should be checked every three to six weeks until it becomes normal.
ββββββββββ
β Final diagnosis:
#High_grade_fatty_liver_disease
π1
Clinical Simulator π©ββπ§ββ pinned Β«https://youtu.be/ktmuY0heYFIΒ»
#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