د. براء عبدالكريم المقادمة،د. ياسمين الخنيزي، د. زهرة الحاج عيسى، د. علي ابو زيد، د. علي الشريف..
و المشاركون:
د. سلطان المدللة، البروفيسور رامي بصطامي، و الاستاذ رامي ولي قوته..
و الشكر للاستشاريين الذين شاركوا في التعليم: د. عثمان الأعرج، د. عبدالله بارضوان، د. نجاح دوبة، د. حسان رمضان، د. صنوبرقاضي، د. بوروسوتام ميسرا، د. مبارك الشمري، و د. نايف الغانم و د. عبد العزيز خان
و الد. حيدر الشخص على مساعدته في تحضير بعض الحالات
و الشكر للدكتور مبارك الشمري (مدير برنامج التدريب) على دعمه و حضوره… و د. محمد المالكي (رئيس القسم) خصوصا على دعمنا بتلبية طلباتنا بالتجهيزات الازمة
Research Team:
Authors:
Dr. Bara AlMakadma, Dr. Yasmin Alkhunaizi, Dr. Zahra Al-Haj Issa, Dr. Ali Buzaid, Dr. Ali Alshareef,
Cotnributors:
Dr. Sultan AlMudallaleh, Prof Rami Bustami, Mr Rami Wali Gotah
Special Thanks:
to the consultant moderators: Dr. Abdullah Baradwan, Dr. Othman AlAraj, Dr Najah Douba, Dr. Hassan Ramadan, Dr Sanober Qazi, Dr. Purosuttam Misra, Dr. Mubarak AlShammari, Dr. Nayef Alghanem, Dr. AbdulAziz Khan
Acknowledgement:
Dr. Haidar AlShakhs for contributing with case preperations, Dr. Mubarak AlShammar (program director), and dr. M. AlMalki (Chairman)
13:00 – 13:30: Introductory video and commentary by consultant
13:35 – 14:40: Case distribution – into 4 groups – group discussion. (timed simulation)
Supervised by Dr. Nayef AlGhanem rheumatology consultant.
14:30 – 14:45: Practical Case,
14:45 – 14:55: Discussion
14:55 – 15:30: Case MCQs.
Topic: Autoimmune vs Treatment Effects!
Field: General Medicine, intensive care, nephrology, psychiatry
Other fields covered:
endocrinology, nephrology, general medicine, diagnostics, hematology, ICU, emergency
Covered completely
Covered partially
Topic:
Intensive care
Topic:
Internal Medicine
Topic:
Nephrology
Topic:
Medical Ethics
Topic:
Topic:
Topic:
Your Task: read the case scenario then:
The following objectives should be covered by you and your team by the end of the case. (place a check-mark on the left-hand side of each pointed completed):
The case is divided into parts with “approach questions” after each part. You will be given timed constraints to discuss in your team and then provide the answer within 2 to 5 minutes as you will be instructed throughout. Roughly 1.5 minutes is awarded for each question to be completed. Answers will be taken verbally. Choose a team representative/ representatives, in each case to talk on behalf of the teams, unless instructed otherwise. You may use any/all resources or electronic devices for this exercise.
#
Topic
Check
1
Understand Glomerulonephritis
2
Nephrotic and nephritic syndromes
3
Interpreting renal function tests
4
Understand Lupus
5
Lupus Nephritis
6
Lupus emergencies
7
Infections with biologic agents
8
The concept of active autoimmune diseases and remission
9
Patient counseling and consent
10
Depression in chronic diseases
Case author (s): Dr. Bara AK AlMakadma, Dr. Yasmin AlKhunaizi, Dr. Zahra AlHaj-Issa, Dr. Sultan AlMudallaleh
Primary references: (cases based upon case reports from):
Case Report by Dr. Bara AK AlMakadma of a patient in KKUH.
Case 8: part 1:
You are covering as the nephrology consulting team’s senior resident.
Today, December 1st 2017 is your first day taking over the consultation service.
You get the following endorsement from the nephrology fellow in the morning meeting (word for word as presented):
“The patient is admitted under rheumatology. He is a 25yo man, known case of Lupus class IV, with low complement levels. His home medications include: CellCept (mycophenolate),
Baseline of proteinuria less than 1 gram. Proteinuria is sub nephrotic:
The patient stopped his CellCept, and so we put him on Imuran (azathioprine). He even refused follow up biopsy.
Anyways, he continues to be sub nephrotic proteinuria.
Currently, his edema is improving; AKI – third spacing induced. LL edema?
He refused cyclophosphamide.
We admitted him on Nov 1st and he was pulsed on steroids and then discharged after improving Cr. AKI improved to baseline of Cr 80 – 90. That was on Nov 8th, 2017. He was admitted again under rheumatology on Nov 20th, 2017 for the same condition. This time, he also had high troponins and with some ECG changes. We sent him for echocardiogram which showed global hypokinemia.
The cardiologist things it looks like ?? viral myocarditis, and in relation to a history of URTI symptoms a week back while he was at home.
Note: patient has some underlying depression. Psychiatry services put him on antidepressants during the last admission, but he denies taking his medications.
Approach Questions: As a large group, we will discuss:
What is the difference between nephrotic and nephritic syndrome? Is there really a difference?
What other data would you like to ask the fellow?
What data would you like to collect from the chart?
What specific areas of patient interview and exam are expected to elucidate?
Outline your thoughts on the patient’s medications?
Should he be returned on previous meds?
Should he receive other medications?
What other services would you like to involve?
Comment on the endorsement above and if it acceptable.
Can you give rituximab with viral myocarditis?
How do you assess lupus nephritis flare?
How do you assess lupus nephritis severity?
Sample answers, and some of the points that should be covered
Must know the time since diagnosis of lupus
Need to know the class of lupus nephritis
Any other manifestations of systemic lupus erythematosus
The current plan from rheumatology
Latest renal biopsy and it’s result
Outline patient’s compliance and social support circle
Involve the ethic committee to over-ride some of the patient’s preferences as he is depressed
Need psychiatry opinion and treatment
Family counselling?
Please note that his complement has always not been congruent with disease activity. Always low.
It is important to ensure that myocarditis is in fact viral vs a secondary organ involvement with active lupus.
we must discuss features of active lupus:
– Proteinuria: compared to baseline
– Increased cr.
Understand variations in complement and their significance in monitoring disease
Identify if concurrent illness is because of active lupus or another è which maybe the reason why complement is low in this patient and is incongruent with disease activity
Discuss the choice of antivirals if any? discuss the choice or rituximab vs other immune modulators in the setting of? viral infection or else (Bacterial otitis)
Case 8: part 2: Hospital Course and Physical Examination
You went to the general medicine ward where the patient is admitted.
You decided to immediately go and see the patient prior to reviewing the chart as to not influence your judgment or create bias. After all, this is your first interview with this patient.
The patient is conscious, oriented, not distressed. He is in his bed. Accompanied by his father, who seems to be an elderly citizen and a nomad.
He was lying in bed and covering his face with his blanket.
You had to call his name twice before he answered and removed the bed-sheet, and looks at you with a blank expression. He seems reluctant to be examined. And slow to move. Prefers to answer your questions with a nod of the head instead of answering. And only when you insist on asking him if has new symptoms he takes a few seconds and says, “my face!”
The patient’s face does not move symmetrically. You decide to start your examination systemically.
General exam is unremarkable.
Cardiovascularexamination reveals normal first and second heart sounds.
Chestexamination is clear
Abdominalexamination is unremarkable.
Neurologicalexamination reveals:
CN: normal except CN 7: he seems to have decreased power and movement on the left side upper and lower face. Intact facial sensation. Intact corneal reflexes.
Otherwise unremarkable neurologic examination.
Prior to leaving the room the patient asks you “when will my face go back to normal?” and he follows with, “can I go home?”
Approach Questions:
How will you answer the patient’s question?
What type of facial palsy is this? Upper or lower motor?
What are the causes of Bells’ palsy? And which one do you think is relevant to this case?
Now write your follow up plan.
(one resident will be chosen randomly to present the data)
Case 8: part 3: Labs: investigate and then interpret
A good physician knows what labs she/he would request at a given time. That depends on the specific patient as well as the clinical picture and disease.
There are things you should always think of depending on certain presentations.
For example, for chronic kidney disease:
Status of Anemia: – Make sure to target Hb 10 to 12 (for ESRD patients) Bone Minerals: – Ca: target 2.2 to 2.5 – P: target 1.1 to 1.7 – ALP, – PTH: should be 2 to 9 times the upper limit of normal Blood pressure: – make sure that BP is not volume overloaded. – hypertension is caused by fluid overload. – make sure that it is less than 130/80 – Make sure you put the dialysis order for each patient as needed. – Check Urinalysis – Check fluid status and see input-output charting Nutrition: – Albumin should be more than 32 – otherwise involve dietitian for high protein diet.
Approach Questions:
What investigations will you look for lupus nephritis:
How to diagnose
How to follow up
Write the name of investigation and what results are expecting for normal, flare, and abnormal.
The definitive diagnosis of lupus is a biopsy, what would you see, and how important is the biopsy in terms of management? And when will you repeat it?
Now, as the PRBTP team for the labs you want and you will be given the results of the labs you ask for.
Case 8: part 4:
At this point, the consultant will give you feedback.
Case Discussion:
Classification of glomerulonephritis:
Lupus nephritis:
Lupus nephritis is staged according to the classification revised by the International Society of Nephrology (ISN) and the Renal Pathology Society (RPS) in 2003, as follows:
Class I – Minimal mesangial lupus nephritis
Class II – Mesangial proliferative lupus nephritis
Class III – Focal lupus nephritis (active and chronic; proliferative and sclerosing)
Class IV – Diffuse lupus nephritis (active and chronic; proliferative and sclerosing; segmental and global)
The Practical Resident Based Teaching Program (PRBTP)
King Saud Medical City (KSMC), Riyadh, KSA,
Internal Medicine
Residency program
PRBTP Team: (as of December 25th, 2017)
1. Dr. Bara AlMakadma
2. Dr. Yasmin AlKhunaizi,
3. Dr. Zahra Al-Haj Issa
4. Dr. Ali Buzaid
5. Dr. Ali Alshareef
6. Dr. Haidar AlShakhs
7. Prof. R. Bustami
Program Director: Dr. Mubarak AlShammary
Special Thanks to the Academic Committee
Special Thanks: to department of medicine and to the chairperson Dr. Mohammad AlMalki (for logistics, funding of audiovisual equipment, and unwavering support)
Case author (s): Dr. Zahra AlHaj-Issa , Dr. Yasmin AlKhunaizi, Dr. Ali Alshareef, Dr. Haidar AlShakhs, Dr. Bara AK AlMakadma
Activity Schedule:
12:30 – 13:30:ECG lecture by Dr. Hatem, cardiology consultant
13:35 – 14:40:Case distribution – into 4 groups – group discussion. (timed simulation)
Supervised by Dr. Najah Douba Medical consultant.
14:30 – 14:45: Practical Case,
14:45 – 14:55:Discussion
14:55 – 15:30: Interactive Video Lecture and feedback
Topic: “Polyendocrine”
Field: General Medicine, intensive care, endocrinology
Other fields covered:
endocrinology, , general medicine, diagnostics, , ICU, emergency
Covered completely
Covered partially
Topic:
Intensive care
Topic:
Internal Medicine
Topic:
Endocrinology
Topic:
Topic:
Topic:
Topic:
Your Task: read the case scenario then:
The following objectives should be covered by you and your team by the end of the case. (place a check-mark on the left-hand side of each pointed completed):
The case is divided into parts with “approach questions” after each part. You will be given timed constraints to discuss in your team and then provide the answer within 2 to 5 minutes as you will be instructed throughout. Roughly 1.5 minutes is awarded for each question to be completed. Answers will be taken verbally. Choose a team representative/ representatives, in each case to talk on behalf of the teams, unless instructed otherwise. You may use any/all resources or electronic devices for this exercise.
Case 7: part 1:
16 years old boy present to our ER with progressive Fatigue and weight loss for 1 month
Approach Questions:
How you will approach this patient in ER?
What is your differential up to here?
Any further questions you would like to ask about to role in/role out your list of differentials?
16 years old boy was in his usual state of health until 1 month when he developed URTI and subsequently started to feel tired all the time, got worse over time. He reports dizziness whenever he stands, with no loss of consciousness. He also reports trouble sleeping and decreased appetite. He lost 12 kg over 1 month. No fever, no night sweats.
Over time, he became weaker and more dependent on his family for daily activity.
He also started to have vomiting 2-3 times per day, food content with preceding nausea. Associated with on/off colicky abdominal pain in variable areas, and 3/ weeks loose bowel motions over these 2 weeks. His mother noticed that his skin got darker
He has positive history of palpitation
Approach Questions:
What do you think we are dealing with right now? (narrow differentials)
Do you have anything else you would like to ask about?
1 week prior to admission, he was seen in a private clinic where he was told that he needs to take thyroid hormone replacement (50mg OD).
He took the medication for 3 days but he got worse; increased vomiting frequency and intensity of abdominal pain. He became weaker & unable to raise himself from the bed. So, he was brought to the hospital.
Medication: Thyroxine 50 mg PO OD and Domperidon
Approach Questions:
What do you think happened here? Can you explain it?
Physical examination showed a young boy with mild pallor, Brittle nails, palmer crease
hyperpigmentation,, hyperpigmented spots on his hard palate and angle of the mouth. Otherwise
unremarkable examinations.
Approach Questions:
What else you want to examine?
Do you think this patient is stable?
What we call the difference between the supine and postural BP measurement in this patient.
Can you now narrow your differential diagnosis?
Do you want to give this patient anything at this time?
Case 7: part 3:
How to approach this patient?
What are the initial investigations?
What do you expect to find in the investigations?
How to differentiate primary from secondary disorder?
What kind of imaging is needed?
Do you need to confirm the diagnosis before starting treatment?
How to treat the acute adrenal crisis?
How to treat adrenal insufficiency outside of crisis?
What important points should be mentioned in patient education?
Why did he deteriorate with Thyroxine?
What Syndrome could explain his condition?
What do you know about this syndrome?
Approach Questions:
Establish diagnosis
For each of the points above, discuss in large group with the consultant what findings are expected in each presentation; in our patient and in the different kinds of presentation of the disease. .
Case 7: part 4:
Understand the human aspect of the disease:
Connect with your patient who suffers from young age
Address compliance issues
Let’s Watch this video and discuss with Dr. Najah!
At this point, the consultant will give you feedback.
Case Discussion:
As a Keen Safe Doctor, You will approach the acute issue first which is the adrenal insufficiency/crisis:
Definition :
Adrenal insufficiency is the clinical manifestation of deficient production or action of glucocorticoids, with or without deficiency also in mineralocorticoids and adrenal androgens.
Types: Primary, Secondary, Tertiary.
EPIDIMIOLOGY:
Prevalence : 12 per 100,000 persons
Incidence : 0.5 per 100,000 persons
Age : may occur at any age , with peak incidence in the fourth decade
Sex:
Autoimmune cause : female predominance
Non autoimmune cause : equal sex distribution
Primary Adrenal insufficiency
Most commonly is of an autoimmune etiology, resulting from chronic destruction of the adrenal cortex
Typical histologic feature is lymphocytic infiltration
Antibodies to adrenal cortical antigens are present early in the disease process 70% sensitivity and highly specificity
Patients with autoimmune adrenal disease are more likely to have polyglandular autoimmune systems causing deficiency of other endocrine glands
Secondary adrenal insufficiency may occur in panhypopituitarism, in isolated failure of ACTH production, in patients receiving corticosteroids (by any route, including high doses of inhaled, intra-articular, or topical corticosteroids), or after corticosteroids are stopped. Inadequate ACTH can also result from failure of the hypothalamus to stimulate pituitary ACTH production, which is sometimes called tertiary adrenal insufficiency.
Panhypopituitarism may occur secondary to pituitary tumors, various tumors, granulomas, and, rarely, infection or trauma that destroys pituitary tissue. In younger people, panhypopituitarism may occur secondary to a craniopharyngioma. Patients receiving corticosteroids for > 4 wk may have insufficient ACTH secretion during metabolic stress to stimulate the adrenals to produce adequate quantities of corticosteroids, or they may have atrophic adrenals that are unresponsive to ACTH. These problems may persist for up to 1 yr after corticosteroid treatment is stopped
When to Suspect Adrenal insufficency?
Clinical features:
Fatigue (84 to 95 percent of patients).in one study of 216 patients, 20 percent had symptoms for more than five years before diagnosis.
Weight loss (66 to 76 percent) ,the weight loss is primarily due to anorexia, but dehydration may contribute. The amount of weight lost can vary from 2 to as much as 15 kg and may not become evident until adrenal failure is advanced
Nausea, vomiting, abdominal pain (49 to 62 percent).
Muscle and joint pain (35 to 40 percent)
1st investigations to order:
-CBC with differential: anemia, lymphocytosis, eosinophilia with primary and secondary insufficiency
-Electrolyte
Hyponatremia is found in 70 to 80 percent of patients.
Hyperkalemia often associated with a mild hyperchloremic acidosis occurs in up to 40 percent of patients due to mineralocorticoid deficiency. So more common in PAI
Hypoglycemia: more common in:
1- infants and children with primary adrenal insufficiency
2- patients with secondary adrenal insufficiency caused by isolated ACTH deficiency
3- patients with type 1 diabetes mellitus who develop adrenal insufficiency
-Serum cortisol :
basal serum cortisol usually tested in early morning (6 AM-9 AM)
You can read about other tests from BMJ or any other reference.
Diagnostic Approach:
Adrenal Crisis (The presentation of our patient)
Adrenal crisis is characterized by
Profound asthenia
Severe pain in the abdomen, lower back, or legs
Peripheral vascular collapse
Renal shutdown with azotemia
Body temperature may be low, although severe fever often occurs, particularly when crisis is precipitated by acute infection.
A significant number of patients with partial loss of adrenal function (limited adrenocortical reserve) appear well but experience adrenal crisis when under physiologic stress (eg, surgery, infection, burns, critical illness). Shock and fever may be the only signs.
Management:
All patients should receive an oral glucocorticoid and mineralocorticoid on diagnosis. In addition, all patients should be empowered by careful education, so that they know when to increase replacement doses appropriately (e.g., when febrile, or vomiting, or in preparation for elective surgical procedures). This may include parenteral administration of glucocorticoids.
The adequacy of glucocorticoid replacement is guided by clinical symptoms. Persistent fatigue is symptomatic of insufficient dosage. Excessive weight gain or facial plethora is symptomatic of over-replacement. Mineralocorticoid dosage is impacted by the mineralocorticoid potency of the glucocorticoid administered and is adjusted based on postural hypotension and serum potassium. Plasma renin activity may be useful when clinical features and other laboratory tests are conflicting.
Adrenal Crisis:
Should be treated immediately, even if an appropriate laboratory diagnosis has not yet been made.
Hydrocortisone sodium succinate: 50-100 mg intravenously every 6-8 hours for 1-3 days
*Use dexamethasone sodium phosphate: 2-4 mg every 6 hours+ Fludocortisone 50 ug daily prior to ACTH stimulation test (not to interfere with the cortisol assay)
Saline should be administered to correct hypotension and dehydration. It is usually necessary to administer 1 L rapidly and a further 2 to 4 L over the first 24 hours, to correct hypotension. Careful monitoring of BP, fluid status, and serum sodium and potassium levels should be maintained.
Glucose should be administered when necessary to correct hypoglycaemia, but care should be taken to avoid worsening hyponatraemia. The use of normal saline supplemented with dextrose 5% is helpful in this regard.
The underlying cause that precipitated the crisis should be sought and treated, and once the patient is stable, normal dosing regimen can be resumed.
Stable and/or after treatment of acute episode
Prednisilone 5 mg PO Once Daily (AM) or Hydrocortisone 15-25 mg PO (2/3 AM, 1/3 early PM)
Oral glucocorticoid and mineralocorticoid replacement therapy is given in physiological doses for life.
Generally, short-acting glucocorticoids such as hydrocortisone are preferred by most physicians.
Mineralocorticoid dose is impacted by mineralocorticoid potency of the glucocorticoid administered.
Excessive mineralocorticoid replacement causes HTN, hypokalaemia, and oedema.
There may be a physiological increase in glucocorticoid and mineralocorticoid requirement during pregnancy. This should be monitored frequently (e.g., every 6 to 8 weeks), and dose adjustments made as appropriate. Since dexamethasone crosses the placenta, alternative glucocorticoids should be prescribed during pregnancy.
In people without adrenal insufficiency, cortisol levels increase physiologically during significant stress such as infection, trauma, and surgery.
Glucocorticoid replacement doses in patients with adrenal insufficiency should be increased accordingly under these circumstances. The usual replacement dose should be doubled while the patient is febrile, and weaned back to replacement over a few days.
If the patient is undergoing a minor procedure, the oral dose should be doubled or tripled for 3 days and then the normal dosing regimen resumed.
During major trauma, infection, or stressful events, intravenous hydrocortisone should be given
Why did our patient deteriorate with Thyroxine:
Remember: Addison disease is also known as “autoimmune hypoadrenalism”
Remember: when a patient has one autoimmune condition: you must rule out others.
Addison’s association is with other endocrinopathies; mainly deficiencies is marked at 10% of patients.
This patient most probably have Autoimmune polyglandular syndrome type 2 which causes dysfunction of multiple endocrine organs such as the thyroid gland, adrenal gland, and pancreas.
Primary adrenal insufficiency is a principal manifestation of APS2. Autoimmune thyroid disease and type 1 diabetes mellitus are also commonly present.
The greatest danger associated with APS2 is treatment of the presenting hypothyroid state without recognition of concomitant hypoadrenalism.
Hypothyroidism reduces cortisol clearance, and the addition of thyroid hormone replacement increases cortisol clearance.
Additionally, hypothyroidism reduces the metabolic rate, thereby, reducing the need for cortisol. The increased metabolic rate accompanying thyroxine replacement increases the requirement for cortisol.
Furthermore, a high serum concentration of TSH in the absence of primary thyroid failure can be a feature of adrenal insufficiency.
The development of an adrenal crisis due to underlying adrenal insufficiency has been reported after the administration of thyroxine replacement therapy to patients initially thought to have only hypothyroidism
Autoimmune polyendocrine syndrome (derived from PassMedicine TM 2017)
There are 4 distinct types of autoimmune polyendocrinopathy syndrome (APS), with type 2 (sometimes referred to as Schmidt’s syndrome) being much more common. APS type 2 has a polygenic inheritance and is linked to HLA DR3/DR4. Patients have Addison’s disease plus either:
type 1 diabetes mellitus
autoimmune thyroid disease
APS type 1 is occasionally referred to as Multiple Endocrine Deficiency Autoimmune Candidiasis (MEDAC). It is a very rare autosomal recessive disorder caused by mutation of AIRE1 gene on chromosome 21 Features of APS type 1 (2 out of 3 needed)
chronic mucocutaneous candidiasis (typically first feature as young child)
Addison’s disease
primary hypoparathyroidism
Vitiligo can occur in both types
Summary of APS types:
Management the patients with thyroid dysfunction
in patients with adrenal insufficiency and hyperthyroidism, double or triple dose of glucocorticoid replacement
in patients with adrenal insufficiency and hypothyroidism, start thyroxine only after concomitant glucocorticoid deficiency has been excluded or treated to avoid acute adrenal insufficiency
—– END OF CASE —–
References:
Real Case – initially presented as a morning report presentation by Dr. Zahra Alhaj Issa, the patient was admitted during 2017 in KSMC under Dr. Najah Douba
Primary references: (cases based upon case reports from): BMJ
Case author (s): Dr. Bara AK AlMakadma, Dr. Yasmin AlKhunaizi, Dr. Ali Buzaid, Dr. Zahra AlHaj-Issa, Dr. Ali Alshareef, Dr. Haidar AlShakhs
Tuesday, November 7th, 2017
Activity Schedule:
12:30 – 13:00:Introduction
13:00 – 13:30: Interactive Video Lecture:
13:30 – 13:35: Break
13:35 – 14:40:Case group distribution & discussion. (timed simulation)
Supervised by Dr. Hassan Ramadan Medical consultant.
14:30 – 14:45: Practical Case,
14:45 – 14:55: Discussion
14:55 – 15:30: Case MCQs.
Topic: “hyponatremia”
Field: General Medicine, intensive care
Other fields covered:
endocrinology, nephrology, general medicine, diagnostics, hematology, ICU, emergency
Covered completely
Covered partially
Topic:
Intensive care
Topic:
Internal Medicine
Topic:
Nephrology
Topic:
Topic:
Topic:
Topic:
Your Task: read the case scenario then:
The following objectives should be covered by you and your team by the end of the case. (place a check-mark on the left-hand side of each pointed completed):
The case is divided into parts with “approach questions” after each part. You will be given timed constraints to discuss in your team and then provide the answer within 2 to 5 minutes as you will be instructed throughout. Roughly 1.5 minutes is awarded for each question to be completed. Answers will be taken verbally. Choose a team representative/ representatives, in each case to talk on behalf of the teams, unless instructed otherwise. You may use any/all resources or electronic devices for this exercise.
#
Topic
Check
1
Definition and Causes of Hyponatremia, Pathophysiology
2
Approach to Hyponatremia
3
Management of Asymptomatic Hyponatremia
4
Management of Symptomatic Hyponatremia (mild/Severe)
5
Complications of Management of Hyponatremia
6
Corrections of Sodium level in case of Hyperglycemia
7
Outline important clinical sequelae understand prevention and treatment of such complications
8
Communicate management plan with concerned staff, and write appropriate medical record
9
10
Case 6: part 1: (Mini-Case 1) You are the medical resident oncall – and you have been called to the emergency department to evaluate the following patient
A 62-year-old, Saudi man presents to the emergency department with: worsening dyspnea and peripheral edema.
Past history: is relevant for prior myocardial infarction followed by cardiomyopathy with an ejection fraction of 20%
Meds: He has been taking:
an ACE inhibitor, beta-blocker, and furosemide, but he ran out of these medications several days ago.
Physical Examination: His BP is 100/60mmHg. High JVP. Chest examination reveals rales to halfway up his lungs, an S3, with a soft systolic murmur. minimally ascetic. Marked peripheral edema to the knee.
Routine electrolyte panel shows a serum sodium level of 125 mmol/L and serum potassium level of 3.6 mmol/L. Serum glucose levels and LFTs are normal
Approach Questions:
History and physical approach: what else would you like to know? What else would you like to examine?
Write your order sheet in the emergency department. (ensure that the following points are ALL addressed in your order sheet):
Any further labs you would like to ask for? What do you expect to find in those labs?
How you will manage this patient (write your order sheet)?
How to approach edema?
Outline the relationship between edema and electrolyte imbalance
Stratify the level of emergency of this patient (which level). Should you admit? decide what to monitor and where to admit. Who are the teams to be involved.
Outline your deficiencies on a blank paper. Determine what would you like to learn? (2 minutes)
Case 6: part 2: Let’s learn more about hyponatremia:
Pull out your computers, and or notebooks, and ensure to know the following materials – as it will be needed to approach the next mini-case.
Case 6: part 3: Mini-Case 2:
A 73-year-old Saudi woman presents to KSMC’s emergency department. Known case of HTN, and depression.
She has fallen down and suffered a hip fracture (right).
She takes
Lisinopril,
chlortalidone (“a diuretic drug used to treat hypertension, originally marketed as Hygroton in the USA. It is described as a thiazide diuretic (or, rather, a thiazide-like diuretic because it acts similarly to the thiazides but does not contain the benzothiadiazine molecular structure”),
and sertraline (“SERTRALINE is used to treat depression. It may also be used to treat obsessive compulsive disorder, panic disorder, post-trauma stress, premenstrual dysphoric disorder or social anxiety.”)
She suffers poor balance since last week. BP is 132/77 mmHg, HR: 85 bpm and regular. On room air. Remainder of the physical examination appears normal. Oral mucosa is moist. Skin turgor is normal. not edematous.
electrolytes panel shows: a serum sodium level of 125 mmol/L and serum potassium level of 3.5 mmol/L. Serum glucose levels and LFTs are normal
Approach Questions:
Interpret the electrolytes panel
Write your working diagnosis and
Write your order sheet.
Case 6: part 4: Mini-Case 3:
“A 76-year-old homeless white man presents to the emergency department after police find him disoriented on the streets in late August. The patient gives little history, but admits to ongoing cough with productive sputum, night sweats/chills, and mild dyspnoea. He proceeds to suffer from a seizure. Vital signs demonstrate an elevated temperature at 38.7°C (101.7°F), a respiration rate of 26 breaths per minute, 94% oxygen saturation (on 3 L of O2), and pulse 87 bpm, with no evidence of orthostatic hypotension.
Physical examination demonstrates a malnourished and dishevelled man in a postictal state. There is no sign of injury to the body. Crackles can be heard at the right lung base. Lab work demonstrates serum sodium of 120 mmol/L (120 mEq/L), serum creatinine of 88 micromol/L (1.0 mg/dL), and negative alcohol and toxicology screens.
CXR demonstrates a large infiltrate in the right lower lung zone, consistent with pulmonary infection or abscess.”
Approach Questions:
Approach to patient (history, exam & labs)?
read CXR?
Interpret findings?
How you will manage this patient? (order sheet)
At this point, the consultant will give you feedback.
Copyrighted materials to Dr. Bara AlMakadma 2017. no reproduction or use of this material outside or personal academic use is allowed without prior written consent.
13:00 – 13:50: Video Presentation/ audiovisual: Background on Metastasis:
Video 2: Metastasis:
13:50: 14:40: Case distribution – into 4 groups – group discussion. (timed simulation)
Supervised by Dr. Abdulaziz Khan, medical oncologist.
14:30-14:45: Practical Session, breaking bad news
14:45-14:55: Discussion
14:55 – 15:30: Case MCQs.
Topic: “Treatment Vs Management” of Disease – Issues in Oncology
Field: Oncology
Other fields covered:
endocrinology, oncology, nephrology, public health, general medicine, , diagnostics, hematology, immunology, ethics, councelling
Covered completely
Covered partially
Topic:
Pathology
Topic:
Internal Medicine
Topic:
Radiology
Topic:
Topic:
Topic:
Topic:
Your Task: read the case scenario then:
The following objectives should be covered by you and your team by the end of the case. (place a check-mark on the left-hand side of each pointed completed):
The case is divided into parts with “approach questions” after each part. You will be given timed constraints to discuss in your team and then provide the answer within 2 to 5 minutes as you will be instructed throughout. Roughly 1.5 minutes is awarded for each question to be completed. Answers will be taken verbally. Choose a team representative/ representatives, in each case to talk on behalf of the teams, unless instructed otherwise. You may use any/all resources or electronic devices for this exercise.
#
Topic
Check
1
Understand the modern approach to the oncology patient
2
How to assess the patient to set management goals
3
When not to treat
4
General medical considerations.
5
The role of screening
6
Patient counseling and breaking bad news.
7
Identify Public health precautions/ impact
8
Ethical considerations.
9
Comparing local data to international data – and learn how obtain them
10
Molecular advances in oncology
Case author: Dr. Bara AK AlMakadma
Co-authors: Dr. Yasmin AlKhunaizi, Dr. Ali Buzaid,
Case 5: part 1:
You are the senior medical resident on duty. It is October 17th 2017.
You are covering the general medicine consultation service when you get a consultation request form the Day Surgical Unity in KSMC (or your hospital).
The consultation request reads:
“60 year old Sudanese male, known case of DM and ?history of TB, -negative for AFB. Status post appendectomy and hemicolectomy for incidental finding of cecal tumor intraoperatively.
The patient is admitted today for evaluation of jaundice, (cholestatic picture) with liver mass for expedited workup. US shows multiple liver lesions. Please note that MRCP done in outpatient setting shows no gross obstruction of bile ducts. Further, the patient does not complain of colicky pain. CT CAP is scheduled for later today. We are referring to you as the patient is having cough with sputum production”
Approach Questions for Group A: Nominate an R1 Resident to answer the following questions: (5 min)
What aspects of history would you like to revisit?
What aspects of history would you like to expand? Explain why? (i.e. what are you thinking of as a differential?)
Now list your differential diagnosis
What other data is needed prior to examination? (e.g. physically see patient’s old prescriptions)
Patient’s chest X-ray obtained that same day – which the nurse opens for you on the computer prior to patient interview:
Case 5: part 2:
Upon further history taking:
As the shrewd medical resident that you are, you did not settle for the brief history described above, and decided to confirm for yourself.
You quickly realized that, although the patient is very well aware of his condition and is passionate about providing you with all information necessary, he is not highly educated and is not fully aware of all the medical and surgical interventions he underwent.
You asked his brother to contact HMG hospital, where the patient performed his laparotomy 5 months ago.
This is the data you gather from your patient interview and physical exam as well as from the medical report are listed below in (disorganized) point form:
The patient is vitally stable on room air.
Physical examination: no gross LAP, chest is clear, vesicular, heart sounds are normal.
o Abdomen is obese, soft, with decreased abdominal tone (mildly lax) and 2/10 rt lower quadrant tenderness. Liver spam is 13 cm. spleen is unpalpable. Otherwise normal (including no sacral nor LL edema)
Otherwise physical examination is normal.
The patient visited HMG 5 months ago with abdominal pain lasting 3 days, paroxysmal and periumbilical. He was admitted as a case of appendicitis
Total admission duration of 1 week. His operation evolved to an appendectomy and hemicolectomy with incidental findings.
The patient was investigated for TB as part of the evaluation of the cecal mass – and AFB, , culture and CPR were all negative. No quantiferon test in HMG at that time. Further the PPD test was negative.
The cough: ongoing for over a year, more in winters, paroxysmal, and exacerbated with perfumes. Occasional white sputum. Today he had sputum production and it was white. For formal diagnosis of asthma before. Not on any inhalers. Not on any meds
No allergies otherwise
No contact with sick patients
No contact with animals
Last trip was to Sudan 6 years ago.
He works as a personal secretary in a home setting and not exposed to chemicals or unusual exposures.
He is married and has two children, a boy and a girl – all of them healthy.
Has been low on appetite since around his surgery today. His weight 5 months ago was 120 kg. His weight upon admission to DSU this morning is 90 kg. Not intended weight loss
No night sweats,
Approach Questions for Group B: Nominate an R1 Resident to answer the following questions: (5 min)
Write your response to the consultation on one page.
Include your assessment and plan. (you will be provided with progress notes)
One resident may volunteer to present their response to the group.
Dr. Khan will then comment on the response and give feedback.
Case 5: part 3:
Investigations:
Approach Question:
Outline the abnormalities above.
Define what you will do next.
Case 5: part 4:
Your Task:
Provide counselling to the patient
Break bad news if needed
At this point, Dr. Abdulaziz Khan will give you feedback.
Case Discussion:
Refer to MKSAP 17 Hematology/ Oncology, Issues in Oncology:
Must know molecular advances in oncology and how that influences treatment and diagnosis.
Performance status:
SPIKES system of breaking bad news.
Know available local resources to you such as those from the Saudi Medical Council
The Practical Resident Based Teaching Program – my baby project…
It took me (and still does todate) an average of 10 hours of weekly work, and many hours of convincing… I had to convince my program director, my colleagues, and even had to do some convincing within our own academic committee (a resident-made group) where I was met with some serious resistance – even from my own friends,luckily, now, I managed to convince them! Sigh! … but what did I expect?
The idea is… new = and inertia is real… people oppose new ideas at first!
To put credit where it is due: the people who have supported the project and contributed to the cases are only three doctors yet far… Dr. AlKhunaizi, Dr. Buzaid and contributions from Dr. AShakhs. I have a strong feeling those three will probably be co-authors, and wish they put their heart in the project. simply because they are great doctors, and I wish to work more alongside them. This is it.. the whole team so far.
one of the tasks ahead will be to recruit more contributors and sign more research participant contracts…. but I digress!
….
Alright, let me try to quickly convince YOU… watch this less than 5 minutes video:
As I came across this video today: my beliefs regarding using the following tools were consolidated:
practical approach
visual approach
audio-visual aids
role-playing
chalk & talk … as well as
video presentations
Further, many people have moved on from classic, didactic teaching… look at how many people subscribe to different channels, websites and online knowledge libraries (and academies, etc.)
I claim that PowerPoints are a boring way to learn, especially when delivered in the purely didactic way – where the presenter does not use the power of features in PowerPoint (and other slides programs) to make their point! Then, I ask myself, “what is the point?” – just give me something to read on my own, and please, for God’s sake, stop wasting my time!
Here are other successful examples of revolutionizing knowledge delivery systems (in our humble opinion):
Some of those examples are in fact what I have elected to use as the video intermissions during our half day releases in our internal medicine teaching program throughout this research & education project.
Let us stop being complacent about our own education.
Let us be economic when it comes to the efficiency of acquiring our own knowledge.
Let us be honest – work hand-in-hand, give credit where it is due, build on each other’s work, stop procrastinating and ultimately become effective, safe confident doctors.
12:30 – 13:30: R1 Crash Crash Course X 2 presentation
13:30 – 13:40: Video Presentation/ audiovisual: Background on HTN and
Atherosclerotic disease:
Video 1:
Video 2:
13:40: 14:40: Case distribution – into 4 groups – group discussion. (timed simulation)
Supervised by Dr. Sanober Shabir Qadi, Medical consultant.
14:30-14:45: Practical demonstration. Mega Code
14:45-14:55: ACLS Mega Code Video demonstration:
14:55 – 15:10: Case MCQs.
———————
15:10 – 15:40: Final Presentation with which the R1 Crash course concludes!
Topic: HTN? No pressure!
Field: general medicine. Cardiovascular
Other fields covered:
endocrinology, pulmonology, nephrology, public health, general medicine, dermatology, diagnostics, hematology
Covered completely
Covered partially
Topic:
Cardiovascular,
Topic:
Electrophysiology and hemodynamics
Topic:
Internal Medicine oncall
Topic:
ACLS
Topic:
Topic:
Topic:
Your Task: read the case scenario then:
Aanswer the following questions about the case with your team: (place a check-mark on the left-hand side of each pointed completed): Roughly 1.5 minutes is awarded for each point to be completed. Answers will be taken verbally. Choose a team representative/ representatives, as per directions in each case to talk on behalf of the teams. You may use any/all resources or electronic devices for this exercise.
#
Topic
Check
1
How to approach in the acute setting
2
HTN definition, an diagnosis
3
Initial treatment – JNC 8 guidelines
4
Definitive investigation, and precautions
5
Interpreting the initial ECG, ABG and CXR
6
Identify Public health precautions/ impact
7
When to consider ACS – and when to implement ACLS guidelines
8
Approach to counselling: patient and community
9
Discuss disease pathogenesis
10
Identify related diseases and their impact on the approach to the patient
You are the internal medicine resident covering the Emergency Department in KSMC
42-year-old black, Ethiopian in origion, heavy smoker, labelled as (Unknown Unknwon in the ER for lack of identification).
Presents with history of untreated hypertension presents with substernal chest pressure.
His symptoms started 1 day prior. The chest discomfort was initially intermittent in nature but has become constant and plagues the anterior chest. He complains of dizziness and some SOB. Apart from a history of hypertension diagnosed 1 year ago, the patient denies any past medical history. There is no clear pain. The patient is not known to have diabetes before.
He is not taking any antihypertensive medications. No known allergies. No recent travel. His father died at the age of 45 after having travelled away from home. He does not know the cause of death.
He denies smoking, or alcohol or drug use. BP is 230/130 mmHg with otherwise normal vital signs and no other significant findings.
ECG:
Approach Questions for Group A: Nominate an R1 Resident to answer the following questions: (5 min)
Read the ECG
You are in Triage: What will you do first?
You are now in the recovery room (patient admitted to ER): what will you do next?
Assuming you successfully approached questions 1 and 2… Now take a history befit of an internist.
Group Discussion: Feedback and criticism from Groups B, C, D (each 2 minutes)
Other ways in which hypertensive emergency can present include neurological symptoms (e.g., stroke, encephalopathy), chest pain signifying cardiac conditions other than infarction or ischaemia (e.g., aortic dissection, pulmonary oedema), or nephrological symptoms (e.g., decreased or absent urine output).
Case 4: part 2:
Upon further history taking:
The patient has had a DVT in his lower limbs 3 weeks ago.
He was admitted to a hospital in Khamis Mushait and given anticoagulation. His admission lasted 2 days. He received 2 other medications that he does not recall.
Approach Questions for Group B: Nominate an R1 Resident to answer the following questions: (5 min)
What is the significance of this history?
What exam parameters will you focus on?
What other tests would you like to have.
Note how in emergency cases there are investigations that are done as part of the initial survey. i.e. in real life scenarios ABG, and ECG +/- CXR may actually result PRIOR TO taking the full patient history, as you would in the ward.
Case 4: part 3:
Physical Exam parameters. Other than vitals mentioned above, normal exam parameters, with equal bilateral pulses
Rapid hematology:
o hematocrit 48%,
o hemoglobin 14.3 g/dl (143 g/L),
Rapid Chemistry:
o white blood cell count 9,000/ μ l,
o glucose 50 mg/dl (25.0 mmol/L),
o urea 5 mg/dl (10.2 mmol/L),
o creatinine: 0.4 mg/dl (123.7 μ mol/L),
o Na+: 142 mEq/L,
o K+: 4.3 mEq/L,
o PO4: 3−2.3 mEq/L (0.74 mmol/L), and
o Cl−: 105 mmol/L.
Atrial Blood Gases:
o Arterial pH was 7.34,
o PO2: 95 mmHg,
o PCO2: 28 mmHg,
o HCO3−: 23 mEq/L, and
o O2 sat: 95%. On 5 leters face mask.
o Lactic acid: 2.8
Approach Question:
Outline the abnormalities above.
Define what you will do next.
A chest X-ray was done: (a real X-ray from a real patient in KSMC from our internal PACS)
Approach Question:
Read the chest X-ray in a comprehensive and appropriate approach.
What would you like to do next?
Case 4: part 3:
The nurse calls you to the room. The patient is profusely sweating. He is drowsy and slowly becoming obtunded.
What is the first thing you should do?
How will you resuscitate the patient?
How do you determine LOC in this case? And does it matter?
Now watch the screen:
III. ACLS Mega Code:
Case 4: part 4:
In the following order sheet: write your orders: (the sheets will be collected for later analysis.) . Each group will submit one Order Sheet. The best will be chosen and then critiqued as a group activity.
At this point, consultant Dr. Sanober Shabir Qadi will give you feedback.
Points of Discussion:
Co morbid infections?
Co-morbid end organ?
Hyper coagulable syndromes?
Possibility of familial syndromes?
Is this patient indicated for cardiac cath?
What do you think you might see should this really be a Wellen’s syndrome?
Answer any questions from audience.
Case Discussion:
Troponin T testing pathway from patients with suspected Acute Coronary Syndrome
Use in patients ≥21 years old presenting with symptoms suggestive of ACS. Do not use if new ST-segment elevation ≥1 mm or new other new EKG changes, hypotension, life expectancy less than 1 year, or noncardiac medical/surgical/psychiatric illness determined by the provider to require admission. See also the HEART Pathway for a validated clinical pathway using the HEART Score.
0-3: 0.9-1.7% risk of adverse cardiac event. In the HEART Score, these patients were discharged. (0.99% retrospective) (1.7% prospective)
4-6: 12-16.6% risk of adverse cardiac event. In the HEART Score, these patients were admitted to the hospital. (11.6% retrospective) (16.6% prospective)
≥7: 50-65% risk of adverse cardiac event. In the HEART Score, these patients were candidates for early invasive measures. (65.2% retrospective) (50.1% prospective)
MACE (Major Adverse Cardiac Events) is defined as: all-cause mortality, myocardial infarction, or coronary revascularization.
Refer to CPR & First Aid website for Emergency Cardiovascular Care:
Figure 1. This is the same as figure 1 from Part 1… here is the correct reading: .Wellens syndrome: symmetrical negative T wave in pre-cordial leads without R loss of R waves can regularly be observed in early anterior ischemia. Many patients with Wellens syndrome / sign turn out to have a critical proximal LAD stenosis.
doctorbara.wordpress.com 