PCL 3: Like Father
1) Polyps (Nicole, Rose & Lukman)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
2) Hemorrhoids (Sam & Kieron)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
3) Trauma (David & Deepak)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
4) Colorectal cancer (Syukriah, Fui Chen, Viran)
a. Epi
b. Patho
c. Signs and symptoms
d. Investigations
e. Treatment
5) Investigations for bleeding per rectal (Shamendri)
Thursday, July 29, 2010
Practical III
Rose - 1
Lukman - 2
Fui Chen - 3
Deepak - 4
David - 5
Syukriah - 6
Kieron - 7
Shamendri - 8
Nicole - 9
Rose - 10
Sam - 11
Lukman - 2
Fui Chen - 3
Deepak - 4
David - 5
Syukriah - 6
Kieron - 7
Shamendri - 8
Nicole - 9
Rose - 10
Sam - 11
Task Delegation
PCL 3: Like Father
1) Polyps (Nicole, Rose)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
2) Hemorrhoids (Sam & Kieron)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
3) Trauma (David & Deepak)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
4) Colorectal cancer (Syukriah, Fui Chen, Viran)
a. Epi
b. Patho
c. Signs and symptoms
d. Investigations
e. Treatment
5) Investigations for bleeding per rectal (Shamendri)
1) Polyps (Nicole, Rose)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
2) Hemorrhoids (Sam & Kieron)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
3) Trauma (David & Deepak)
a. Patho
b. Signs and symptoms
c. Investigations
d. Treatment
4) Colorectal cancer (Syukriah, Fui Chen, Viran)
a. Epi
b. Patho
c. Signs and symptoms
d. Investigations
e. Treatment
5) Investigations for bleeding per rectal (Shamendri)
Wednesday, July 28, 2010
Deepak's Last Week Stuff
Goal of Treatment
Bring the symptoms under control.
Heal the esophagus.
Manage or prevent complications.
Maintain the symptoms of GERD in remission.
1st Line: Changes to Lifestyle
Position
Eating Manner
Diet
Weight Loss
Smoking Cessation
Simple Antacids (over-the-counter)
Avoiding NSAIDS
2nd Line: Medical Intervention
CLASS MOA EXAMPLES DOSAGE
Alginate –containing Antacids Neutralise stomach acid,
forms foam raft. Ca, Mg, Al containing antacids As and when necessary (after meals)
H2 Antagonists Acid supression cimetidine, ranitidine, famotidine 30 minutes before meals
Proton Pump Inhibitors Reduce gastic acid production by up to 90% omeprazole, rabeprazole, lansoprazole, pantoprazole, esomeprazole Severe:
Twice daily & prolonged for years
Pro-Motility Drugs Stimulate muscles of GIT metoclopramide 30 minutes before meals,
at bedtime
3rd Line: Surgical Intervention
The operation used most often for GERD is called fundoplication. The top of the stomach is wrapped around the lower end of the oesophagus, tightening the oesophageal sphincter.
http://www.youtube.com/watch?v=9bnIuKiHdDE
By Deepak
Bring the symptoms under control.
Heal the esophagus.
Manage or prevent complications.
Maintain the symptoms of GERD in remission.
1st Line: Changes to Lifestyle
Position
Eating Manner
Diet
Weight Loss
Smoking Cessation
Simple Antacids (over-the-counter)
Avoiding NSAIDS
2nd Line: Medical Intervention
CLASS MOA EXAMPLES DOSAGE
Alginate –containing Antacids Neutralise stomach acid,
forms foam raft. Ca, Mg, Al containing antacids As and when necessary (after meals)
H2 Antagonists Acid supression cimetidine, ranitidine, famotidine 30 minutes before meals
Proton Pump Inhibitors Reduce gastic acid production by up to 90% omeprazole, rabeprazole, lansoprazole, pantoprazole, esomeprazole Severe:
Twice daily & prolonged for years
Pro-Motility Drugs Stimulate muscles of GIT metoclopramide 30 minutes before meals,
at bedtime
3rd Line: Surgical Intervention
The operation used most often for GERD is called fundoplication. The top of the stomach is wrapped around the lower end of the oesophagus, tightening the oesophageal sphincter.
http://www.youtube.com/watch?v=9bnIuKiHdDE
By Deepak
Tuesday, July 27, 2010
Heptitis Investigations
Prior to ordering tests for hepatitis, the physician should consider the patient’s history, age, risk
factors, vaccination status and any available previous hepatitis test results.
It must be recognized that an established infection with one hepatitis virus does not exclude co- or superinfection with other hepatitis viruses or other agents such as cytomegalovirus or Epstein-Barr virus, although such dual infections are considered uncommon.
Other possibilities to be considered include hepatotoxic drugs including herbal medicines.
Risk factors for viral hepatitis include:
• Substance abuse (e.g. injection drug use, snorting cocaine)
• High-risk sexual activity (e.g. men who have sex with men, traumatic sex)
• Multiple sexual partners
• A sexual partner with viral hepatitis
• Travel to high-risk hepatitis endemic areas or exposure during a local outbreak
• Household contact with an infected person especially if personal items (e.g. razors, toothbrushes,
nail clippers) are shared
• Attendance at daycare
• History of a transfusion-dependent illness
• Needle-stick injury or other occupational exposure (e.g. healthcare workers)
• Receipt of blood products prior to 1990
• Newborn of infected mother
• Tattoos and body piercing
• Contaminated food or water (hepatitis A only)
Role of serology in hepatitis management
•Serology involves the study of seroactive substances for the purpose of diagnosis and
management of diseases
•Such substances may include antigens and antibodies.
•The presence and time of detection of these substances are essential in hepatological
Infectology
Hepatitis A
•Anti HAV:
▫Detectable at onset of symptoms (IgM)
▫Persists for lifetime hence not very useful clinically (IgG)
•IgManti HAV indicates recent infection. Could remain +ve4-6months post infection.
Hepatitis B
• Serologic markers include:
▫ Hep B surface antigen (HBsAg)
Detectable in large quantities in serum
Indicates acute infection and high infectivity
Appears in blood late incubation period and disappears within 3-4 wks but may persist up to 6mths
▫ Anti HBs
Indicates past infection with and immunity to HBV (if assoc. with anti HBc), presence of passive antibody from HBIG,or immune response from HBV vaccine
• Hep B core antigen (HBcAg)
• Anti HBc: of 2 types
▫ IgM
Appears after about 2 mths and may persist till 7th mth.
Indicates acute infection
▫ IgG
Indicates chronic infection
• HBe Ag
▫ Circulating form of HBcAg
▫ A marker of viral replication and infectivity
▫ Appears transiently at onset of infection and lasts 1-3mths
▫ Associated with HBV replication and indicates high titre and infectivity of serum
• Anti-HBe
▫ Appears from 10th wek
▫ Presence in serum of HBsAg carrier suggests lower titre of HBV
• Most sensitive test is detection of HBV DNA in serum though not generally required for routine diagnosis
• HCV:
▫ Anti-HCV, for chronic infections
▫ Serum PCR
• HDV:
▫ Anti HDV (IgG & IgM)
• HEV:
▫ Anti HEV
Conclusion
• Viral hepatitis is a common cause of CLD in this environment.
• Healthworkers are particularly at risk of infection
• Understanding the basis for serological investigations of viral hepatitis improves diagnosis, management, prognostication as well as prevention of the disease and its complications.
factors, vaccination status and any available previous hepatitis test results.
It must be recognized that an established infection with one hepatitis virus does not exclude co- or superinfection with other hepatitis viruses or other agents such as cytomegalovirus or Epstein-Barr virus, although such dual infections are considered uncommon.
Other possibilities to be considered include hepatotoxic drugs including herbal medicines.
Risk factors for viral hepatitis include:
• Substance abuse (e.g. injection drug use, snorting cocaine)
• High-risk sexual activity (e.g. men who have sex with men, traumatic sex)
• Multiple sexual partners
• A sexual partner with viral hepatitis
• Travel to high-risk hepatitis endemic areas or exposure during a local outbreak
• Household contact with an infected person especially if personal items (e.g. razors, toothbrushes,
nail clippers) are shared
• Attendance at daycare
• History of a transfusion-dependent illness
• Needle-stick injury or other occupational exposure (e.g. healthcare workers)
• Receipt of blood products prior to 1990
• Newborn of infected mother
• Tattoos and body piercing
• Contaminated food or water (hepatitis A only)
Role of serology in hepatitis management
•Serology involves the study of seroactive substances for the purpose of diagnosis and
management of diseases
•Such substances may include antigens and antibodies.
•The presence and time of detection of these substances are essential in hepatological
Infectology
Hepatitis A
•Anti HAV:
▫Detectable at onset of symptoms (IgM)
▫Persists for lifetime hence not very useful clinically (IgG)
•IgManti HAV indicates recent infection. Could remain +ve4-6months post infection.
Hepatitis B
• Serologic markers include:
▫ Hep B surface antigen (HBsAg)
Detectable in large quantities in serum
Indicates acute infection and high infectivity
Appears in blood late incubation period and disappears within 3-4 wks but may persist up to 6mths
▫ Anti HBs
Indicates past infection with and immunity to HBV (if assoc. with anti HBc), presence of passive antibody from HBIG,or immune response from HBV vaccine
• Hep B core antigen (HBcAg)
• Anti HBc: of 2 types
▫ IgM
Appears after about 2 mths and may persist till 7th mth.
Indicates acute infection
▫ IgG
Indicates chronic infection
• HBe Ag
▫ Circulating form of HBcAg
▫ A marker of viral replication and infectivity
▫ Appears transiently at onset of infection and lasts 1-3mths
▫ Associated with HBV replication and indicates high titre and infectivity of serum
• Anti-HBe
▫ Appears from 10th wek
▫ Presence in serum of HBsAg carrier suggests lower titre of HBV
• Most sensitive test is detection of HBV DNA in serum though not generally required for routine diagnosis
• HCV:
▫ Anti-HCV, for chronic infections
▫ Serum PCR
• HDV:
▫ Anti HDV (IgG & IgM)
• HEV:
▫ Anti HEV
Conclusion
• Viral hepatitis is a common cause of CLD in this environment.
• Healthworkers are particularly at risk of infection
• Understanding the basis for serological investigations of viral hepatitis improves diagnosis, management, prognostication as well as prevention of the disease and its complications.
Cholecystitis
• Inflammation of gall bladder
• Cholelithiasis
o Gall stones
o Formed in biliary tract
Cholesterol
Bile pigment
• Caused by cholesterol crystallization from gall bladder bile
o Cholesterol supersaturation of bile
o Crystallization promoting factors within bile
o Motility of gall bladder
• Bile pigment stones
o Black
o Brown
• Cholecystitis caused by obstruction to gall bladder emptying.
• Caused by obstruction of the cystic or common bile duct by a stone migrating from the gall bladder.
o Obstruction results in increased glandular secretion leading to progressive distension of the gall bladder.
• Symptoms
o Severe, steady pain in the epigastric region that then localises to the upper right quadrant.
o Pain gets worse with deep breaths
o The pain often radiates to the tip of the right scapula.
o Fever, sweating, chills
o Loss of appetite, abdominal bloating
o Jaundice
By Kieron
• Inflammation of gall bladder
• Cholelithiasis
o Gall stones
o Formed in biliary tract
Cholesterol
Bile pigment
• Caused by cholesterol crystallization from gall bladder bile
o Cholesterol supersaturation of bile
o Crystallization promoting factors within bile
o Motility of gall bladder
• Bile pigment stones
o Black
o Brown
• Cholecystitis caused by obstruction to gall bladder emptying.
• Caused by obstruction of the cystic or common bile duct by a stone migrating from the gall bladder.
o Obstruction results in increased glandular secretion leading to progressive distension of the gall bladder.
• Symptoms
o Severe, steady pain in the epigastric region that then localises to the upper right quadrant.
o Pain gets worse with deep breaths
o The pain often radiates to the tip of the right scapula.
o Fever, sweating, chills
o Loss of appetite, abdominal bloating
o Jaundice
By Kieron
Gastroesophageal Reflux Disease
Gastroesophageal reflux is a normal physiologic phenomenon experienced intermittently by most people, particularly after a meal. Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing symptoms with or without associated esophageal mucosal injury (ie, esophagitis).
Pathophysiology
The physiologic and anatomic factors that prevent the reflux of gastric juice from the stomach into the esophagus include the following:
• The lower esophageal sphincter (LES) must have a normal length and pressure and a normal number of episodes of transient relaxation (relaxation in the absence of swallowing).
• The gastroesophageal junction must be located in the abdomen so that the diaphragmatic crura can assist the action of the LES, thus functioning as an extrinsic sphincter. The presence of a hiatal hernia disrupts this synergistic action and can promote reflux (see image below).
•
Barium swallows indicating hiatal hernia.
• Esophageal clearance must be able to neutralize the acid refluxed through the LES. (Mechanical clearance is achieved with esophageal peristalsis. Chemical clearance is achieved with saliva.)
• The stomach must empty properly.
Abnormal gastroesophageal reflux is caused by the abnormalities of one or more of the following protective mechanisms:
• A functional (frequent transient LES relaxation) or mechanical (hypotensive LES) problem of the LES is the most common cause of gastroesophageal reflux disease (GERD).
• Certain foods (eg, coffee, alcohol), medications (eg, calcium channel blockers, nitrates, beta-blockers), or hormones (eg, progesterone) can decrease the pressure of the LES.
• Obesity is a contributing factor in gastroesophageal reflux disease (GERD), probably because of the increased intra-abdominal pressure.
From a therapeutic point of view, informing patients that gastric refluxate is made up not only of acid but also of duodenal contents (eg, bile, pancreatic secretions) is important.
By Shamendri
Gastroesophageal reflux is a normal physiologic phenomenon experienced intermittently by most people, particularly after a meal. Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing symptoms with or without associated esophageal mucosal injury (ie, esophagitis).
Pathophysiology
The physiologic and anatomic factors that prevent the reflux of gastric juice from the stomach into the esophagus include the following:
• The lower esophageal sphincter (LES) must have a normal length and pressure and a normal number of episodes of transient relaxation (relaxation in the absence of swallowing).
• The gastroesophageal junction must be located in the abdomen so that the diaphragmatic crura can assist the action of the LES, thus functioning as an extrinsic sphincter. The presence of a hiatal hernia disrupts this synergistic action and can promote reflux (see image below).
•
Barium swallows indicating hiatal hernia.
• Esophageal clearance must be able to neutralize the acid refluxed through the LES. (Mechanical clearance is achieved with esophageal peristalsis. Chemical clearance is achieved with saliva.)
• The stomach must empty properly.
Abnormal gastroesophageal reflux is caused by the abnormalities of one or more of the following protective mechanisms:
• A functional (frequent transient LES relaxation) or mechanical (hypotensive LES) problem of the LES is the most common cause of gastroesophageal reflux disease (GERD).
• Certain foods (eg, coffee, alcohol), medications (eg, calcium channel blockers, nitrates, beta-blockers), or hormones (eg, progesterone) can decrease the pressure of the LES.
• Obesity is a contributing factor in gastroesophageal reflux disease (GERD), probably because of the increased intra-abdominal pressure.
From a therapeutic point of view, informing patients that gastric refluxate is made up not only of acid but also of duodenal contents (eg, bile, pancreatic secretions) is important.
By Shamendri
Investigations of Cholecystitis
History
EPIGASTRIC pain radiating to the RIGHT HYPOCHONDRIUM, may radiate to tip of scapula
Quality: Colicky --> Constant
Associated symptoms: Nausea, vomiting, fever
Physical Examination
Fever, tachycardia, jaundice
Maximal tenderness in right hypochondrium with guarding & rebound
+ve Murphy's sign
Investigations
Blood tests: FBC, ESR, bilirubin, alkaline phosphatase, serum aminotransferase
Urinalysis
Pregnancy test
Abdominal ultrasound
CT scan
Hepatobiliary scintigraphy
EPIGASTRIC pain radiating to the RIGHT HYPOCHONDRIUM, may radiate to tip of scapula
Quality: Colicky --> Constant
Associated symptoms: Nausea, vomiting, fever
Physical Examination
Fever, tachycardia, jaundice
Maximal tenderness in right hypochondrium with guarding & rebound
+ve Murphy's sign
Investigations
Blood tests: FBC, ESR, bilirubin, alkaline phosphatase, serum aminotransferase
Urinalysis
Pregnancy test
Abdominal ultrasound
CT scan
Hepatobiliary scintigraphy
Summary of TREATMENT AND MANAGEMENT OF CHOLECYSTITIS
Medical care
• Bowel rest – no eat & drink
• IV hydration
• Nasogastric suction- keep stomach empty & reduce fluid accumulation in intestine
• Anti-emetics (list of drugs and their MOA)
• IV antibiotics (list of drugs and their MOA)
• IV analgesic (pain reliever) (list of drugs and their MOA)
• Daily stimulation of gallbladder contraction by IV CCK (cholecystokinin)
Surgery (cholecystectomy)
• Open surgery
• Laparoscopic
Medical care
• Bowel rest – no eat & drink
• IV hydration
• Nasogastric suction- keep stomach empty & reduce fluid accumulation in intestine
• Anti-emetics (list of drugs and their MOA)
• IV antibiotics (list of drugs and their MOA)
• IV analgesic (pain reliever) (list of drugs and their MOA)
• Daily stimulation of gallbladder contraction by IV CCK (cholecystokinin)
Surgery (cholecystectomy)
• Open surgery
• Laparoscopic
Thursday, July 22, 2010
Abdomen II- Peritoneal Sac
1. Abdominal in relation to the Anterior Abdominal Wall - Sham & Rosy
2. Peritoneal Cavity & Reflections
Sam- (2.1-2.2)
Kieron- (2.3-2.4)
Fui Chen- (2.5-2.6)
3. GIT
Nicole - 3.1
Lukman - (3.2-3.4)
4. Nerves - David & Nicole
5. Vessels
Deepak (5.1 & 5.2)
Syukriah (5.3-5.4)
6 & 7 -Viran
2. Peritoneal Cavity & Reflections
Sam- (2.1-2.2)
Kieron- (2.3-2.4)
Fui Chen- (2.5-2.6)
3. GIT
Nicole - 3.1
Lukman - (3.2-3.4)
4. Nerves - David & Nicole
5. Vessels
Deepak (5.1 & 5.2)
Syukriah (5.3-5.4)
6 & 7 -Viran
SHARIFAH’S NIGHT OUT
Demography: Female, married, 58 yo, housewife, 3 grown up children (2 d 1 s), slightly overweight (BMI=25)
CC: Epigastric pain
Over indulgence, nausea
HPI: When- on and off, worse last four days, frequent on few days ago, severe pain
Where-Middle
Quality- radiated to R side of the chest (tenderness), severe
Quantity-on off, 3-7
Better-No
Worse-Lie down, food
Associated symptoms-fever, feel like vomiting
Belief-heart attack
Fam Hx: father cholecystectomy, parents died due to old age,
Past Med Hx:
Diet: always kenduri
Social smoker- 3-4 cigarettes/day
Medication: No
Allergy: No
Travel: to Kelantan
O&G: 10 years post menopausal
Investigation: FBC, Urinalysis normal, liver function, cholesterol level (raised 5-10%), ultrasound, endoscopy, ECG normal, cardiac enzyme, 37.2oc, HR 80/min, BP 140/90, RR 12, ESR slightly raised, bilirubin borderline, alkaline phosphotase raised mildly, blood glucose normal, amylase normal
Murphy’s sign-a bit painful
Differential Diagnosis:
1. Cholecystitis
2. Hepatitis
3. Pancreatitis
4. Gastritis
5. Gastroesophageal reflux
6. Stomach cancer
7. MI
Learning issues
1) Overview of the anatomy of the GIT (Sam, Nic)
2) Pathophysio of chole, hep and GERD. Signs & symptoms. What are these 3 things? (Shamzi-GERD, Kieron- Chole, Luk-Hep)
3) Treatment and management (Syukriah- Chole, David- Hep, Deepak- GERD)
4) Investigations (Rosy- Chole, FC-GERD, Vir-Hep) *PCL is a bit different nowadays, we have to cover all 3 diseases, so just check out on which one you’re doing!
Demography: Female, married, 58 yo, housewife, 3 grown up children (2 d 1 s), slightly overweight (BMI=25)
CC: Epigastric pain
Over indulgence, nausea
HPI: When- on and off, worse last four days, frequent on few days ago, severe pain
Where-Middle
Quality- radiated to R side of the chest (tenderness), severe
Quantity-on off, 3-7
Better-No
Worse-Lie down, food
Associated symptoms-fever, feel like vomiting
Belief-heart attack
Fam Hx: father cholecystectomy, parents died due to old age,
Past Med Hx:
Diet: always kenduri
Social smoker- 3-4 cigarettes/day
Medication: No
Allergy: No
Travel: to Kelantan
O&G: 10 years post menopausal
Investigation: FBC, Urinalysis normal, liver function, cholesterol level (raised 5-10%), ultrasound, endoscopy, ECG normal, cardiac enzyme, 37.2oc, HR 80/min, BP 140/90, RR 12, ESR slightly raised, bilirubin borderline, alkaline phosphotase raised mildly, blood glucose normal, amylase normal
Murphy’s sign-a bit painful
Differential Diagnosis:
1. Cholecystitis
2. Hepatitis
3. Pancreatitis
4. Gastritis
5. Gastroesophageal reflux
6. Stomach cancer
7. MI
Learning issues
1) Overview of the anatomy of the GIT (Sam, Nic)
2) Pathophysio of chole, hep and GERD. Signs & symptoms. What are these 3 things? (Shamzi-GERD, Kieron- Chole, Luk-Hep)
3) Treatment and management (Syukriah- Chole, David- Hep, Deepak- GERD)
4) Investigations (Rosy- Chole, FC-GERD, Vir-Hep) *PCL is a bit different nowadays, we have to cover all 3 diseases, so just check out on which one you’re doing!
Monday, July 19, 2010
PCL Week 1 Sem 4: Why am I overweight?
Bio: Sushila, Indian, mid 20s, female, accountant, smoker, overweight.
CC: Constant lethargy & fatigue.
Associated symptoms: -
Lifestyle: Constant dieter, smoker, leads a sedentary lifestyle, stressed? Low confidence & esteem.
Family history: Overweight, culture
Issues
1. Overweight & Obesity – Definition & Epidemiology (How common? Classifications?) (Lukman)
2. Differential: Hypothyroidism, Cushing’s (steroid consumption) (Shamzi)
3. BMI & Waist Circumference, Hip-waist ratio, indicators of overweight and obesity (Asians etc.) (Deepak)
4. Risk factors for overweight & obesity. (David)
5. Complications for overweight & obesity. (Viran)
6. Treatment and Management: Lifestyle change, diet change, Medication & surgery (CPG for obesity, www.ifnotdieting.com) (Nicole & Kieron)
7. Diets – Different types, Normal calorie allowance (Syukriah)
8. Recommended weight loss (per week), Maintenance, (Fui Fui)
9. How society perceives the overweight (and what is an ideal physique)? The patient (Sam & Rose)
Bio: Sushila, Indian, mid 20s, female, accountant, smoker, overweight.
CC: Constant lethargy & fatigue.
Associated symptoms: -
Lifestyle: Constant dieter, smoker, leads a sedentary lifestyle, stressed? Low confidence & esteem.
Family history: Overweight, culture
Issues
1. Overweight & Obesity – Definition & Epidemiology (How common? Classifications?) (Lukman)
2. Differential: Hypothyroidism, Cushing’s (steroid consumption) (Shamzi)
3. BMI & Waist Circumference, Hip-waist ratio, indicators of overweight and obesity (Asians etc.) (Deepak)
4. Risk factors for overweight & obesity. (David)
5. Complications for overweight & obesity. (Viran)
6. Treatment and Management: Lifestyle change, diet change, Medication & surgery (CPG for obesity, www.ifnotdieting.com) (Nicole & Kieron)
7. Diets – Different types, Normal calorie allowance (Syukriah)
8. Recommended weight loss (per week), Maintenance, (Fui Fui)
9. How society perceives the overweight (and what is an ideal physique)? The patient (Sam & Rose)
Subscribe to:
Comments (Atom)