GENERAL MEDICINE AUGUST 2021 BIMONTHLY BLENDED ASSESSMENT

  QUESTION 1

Testing peer review competency;

https://2018-21batchpgy3gmpracticals.blogspot.com/2021/08/18100006003-case-presentations.html?m=1

Review: The long case on Polyarthritis leading to Acute Glomerulonephritis and the history was well presented and detailed enough to rule out the case and even the analysis of signs and symptoms were discussed from pathology basis which made easy for me to point towards the diagnosis and well explained differential diagnosis and I felt its worthy to go through the lengthy but detailed case.

Coming to Short cases , one is Idiopathic Parkinson's Disease Stage 1 with denovo HTN  

 and the other is Iatrogenic Cushings Syndrome the both cases presented well especially the second one where the photographs showed a great explaining in prognosis of the disease.

  

QUESTION 2

Testing scholarship competency of the examinees; ability to read comprehend, analyze, reflect upon and discuss captured patient centered data. Analyze the above linked long and short cases patient data by first preparing a problem list for each patient in order of perceived priority and then discuss the diagnostic and therapeutic uncertainty around solving those problems. 

Long case:

• Had severe joint pains, which were initially asymmetric and gradually became bilaterally symmetrical and involving the small joints of his hands and wrist. The joint pains were associated with significant local edema, and painful limitation of movements, which made his job (stonemasonry) difficult. 
• Debilitating early morning pains and limitation of movements in his hands, wrists and feet, which usually lasts for about an hour, He reported that the pains and limitation of movements improved with activity, with gradual reduction in edema of joints.
• Joint symptoms gradually progressed in severity, now also involving several large joints
• Recently, has burning sensation in his eyes with increased tearing but no visual deficits. He also reported for the past 1 year, he developed subcutaneous swellings in the proximal joints of his fingers
• 3 day history of anasarca, frothy urine and gradually decreasing urine output.

this shows that Anasarca and frothy urine with decreasing urine output suggest a renal pathology. Proteinuria causing anasarca likely due to glomerular pathology. Pointing  acute development of glomerulonephritis secondary to poorly treated bilaterally symmetrical polyarthritis.

Short case 1:

• stiffness in his wrists (Right>Left), which has now ascended to his elbows. 
•  same involuntary movements also started appearing in his left hand. 
• difficulty in taking stairs up, in that he feels he sometimes might lose balance
• Involuntary movements - Resting tremors of Right upper limb , 3-4Hz, high amplitude.
  Gait - Reduced arm swing.
• Cog wheel rigidity at wrist joint
• Clarity in speech is decreased and plains of having ugly handwriting recently.

The diagnosis stated as Idiopathic Parkinson's Disease Stage 1 with denovo HTN , Multiple System Atrophy - Parkinsonian Type (MSA-P).

Short case 2:

• Itchy Ring leisons over arms ,abdomen ,thigh and groin since 1 and half year .
• Purple stretch marks all over abdomen ,lower back ,upper limbs ,thighs since 1 year .
• Abdominal distension and facial puffiness since 6 months.
• Pedal edema 
• Low back ache 
• Feeling low , not feeling to talk to anyone.
• Weight gain and decreased libido 
• Loss of libido and erectile dysfunction
• Thin skin present . 
• Poor healing noticed over leg ulcers and easy bruising noted .
• Acne present over face .
• Acanthosis nigrans noted over neck.
• GYNECOMASTIA PRESENT .
• Buffalo hump present .
• Sparse scalp hair

The above signs, symptoms and on analysing the prognosis time to time and supports the diagnosis of the exogenous Cushings Syndrome .But the dilemma of endogenous Cushings syndrome is raised due to slow response to treatment .And the patient also have facing social stigma and avoiding social interactions - moderate depression -taking psychiatry counseling .

QUESTION 3

Testing competency in "Evidence based medicine": Include the review of literature around sensitivity and specificity of the diagnostic interventions mentioned and same around efficacy of the therapeutic interventions mentioned.

Review : The longcase is case of Acute glomerulonephritis secondary to poorly treated Bisymmetrical Polyarthritis and the pathophysiology is well explained symptomatically.

Signs and symptoms of rheumatoid arthritis

In most patients with RA, onset is insidious, often beginning with fever, malaise, arthralgias, and weakness before progressing to joint inflammation and swelling.

Signs and symptoms of RA may include the following:

• Persistent symmetric polyarthritis (synovitis) of hands and feet (hallmark feature)
• Progressive articular deterioration
• Extra-articular involvement
• Difficulty performing activities of daily living (ADLs)
• Constitutional symptom

The physical examination should address the following:

• Upper extremities (metacarpophalangeal joints, wrists, elbows, shoulders
• Lower extremities (ankles, feet, knees, hips)
• Cervical spine

During the physical examination, it is important to assess the following:

• Stiffness
• Tenderness
• Pain on motion
• Swelling
• Deformity
• Limitation of motion
• Extra-articular manifestations
• Rheumatoid nodules

In the given case the Acute GN is secondary to the Arthritis which can be explained as 

Glomerular lesions in acute GN are the result of glomerular deposition or in situ formation of immune complexes. On gross appearance, the kidneys may be enlarged up to 50%. Histopathologic changes include swelling of the glomerular tufts and infiltration with polymorphonucleocytes. 

Short cases 

  Parkinson disease is a clinical diagnosis. No laboratory biomarkers exist for the condition, and findings on routine magnetic resonance imaging and computed tomography scans are unremarkable.

Clinical diagnosis requires the presence of 2 of 3 cardinal signs:

• Resting tremor

• Rigidity

• Bradykinesia

Treatment :

The goal of medical management of Parkinson disease is to provide control of signs and symptoms for as long as possible while minimizing adverse effects.

Usually provides good control of motor signs of Parkinson disease for 4-6 years

Levodopa/carbidopa: The gold standard of symptomatic treatment

Monoamine oxidase (MAO)–B inhibitors: Can be considered for initial treatment of early disease

Other dopamine agonists (eg, ropinirole, pramipexole): Monotherapy in early disease and adjunctive therapy in moderate to advanced disease.

Exogenous Cushing syndrome

Cushing syndrome, refers to signs and symptoms  caused by excess free plasma glucocorticoids. Excess glucocorticoids can be from increased endogenous production or prolonged exposure to exogenous use of glucocorticoid products. While endogenous Cushing syndrome is a rare disease, iatrogenic (drug-related or exogenous) Cushing syndrome from glucocorticoid products is commonly seen in clinical practice. This article will focuses on iatrogenic, or drug-related, Cushing syndrome.

 Drugs that have been reported to result in hypercortisolism are glucocorticoids, megestrol  acetate, and herbal preparations that contain glucocorticoids.

Management of Cushing syndrome

The treatment for exogenous Cushing syndrome is gradual withdrawal of the causative drug, with the aim of discontinuing the causative drug if possible. An individual with hypothalamic-pituitary-adrenal (HPA)–axis suppression cannot increase steroid production appropriately during a medical illness or other stress and should receive stress-dose steroids to avoid adrenal crisis.

Endogenous cushing syndrome

Endogenous glucocorticoid overproduction or hypercortisolism that is independent of ACTH is usually due to a primary adrenocortical neoplasm (most commonly an adenoma and rarely a carcinoma). Bilateral micronodular hyperplasia (primary pigmented nodular adrenocortical disease) and macronodular hyperplasia are rare causes of Cushing syndrome.

Ectopic cortisol secretion from a case of ovarian carcinoma has been reported as a cause of ACTH-independent Cushing syndrome.

ACTH level in ACTH-independent Cushing syndrome is low due to the negative feedback to pituitary corticotroph cells from a high level of serum cortisol. ACTH-dependent Cushing syndrome is characterized by elevated ACTH levels. Elevated ACTH levels are usually due to an anterior pituitary tumor, which is classic Cushing disease (60-70%). Nonpituitary ectopic sources of ACTH, such as small-cell lung carcinoma (oat cell carcinoma), carcinoid tumor, medullary thyroid carcinoma, or other neuroendocrine tumors can result in high ACTH levels and sequentially hypercortisolism.

Treatment of Cushing syndrome is directed by the primary cause of the syndrome. In general, therapy should reduce the cortisol secretion to normal to reduce the risk of comorbidities associated with hypercortisolism. The treatment of choice for endogenous Cushing syndrome is surgical resection of the causative tumor. The primary therapy for Cushing disease is transsphenoidal surgery, and the primary therapy for adrenal tumors is adrenalectomy.

QUESTION 4

Share the link to your own case report this month of a patient that you connected with and engaged while capturing his her sequential life events before and after the illness and clinical and investigational images along with your discussion of that case.

https://soumyamenda80.blogspot.com/2021/08/70-year-old-male-with-epigastric-pain.html

The above link is of log done by me and the case of CRF . The sequential events are as 

• 4 years back SOB, Pedal edema for while and admitted to hospital and treated
• 3 years back developed Back pain which was on and off and was on medication [RMP Dr.]
• Since 2 months he has Back pain and fever
• Since 1 month he developed SOB, Pedal edema and increase in severity from 10 days
• Burning micturition and decrease in urine output since 4 day

He also had TB 20 years back.
Diagnosis : CHRONIC RENAL FAILURE AND THROMBOCYTOPENIA

Chronic kidney disease (CKD)—or chronic renal failure (CRF), as it was historically termed—is a term that encompasses all degrees of decreased kidney function, from damaged–at risk through mild, moderate, and severe chronic kidney failure.

The guidelines define CKD as either kidney damage or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for at least 3 months. Whatever the underlying etiology, once the loss of nephrons and reduction of functional renal mass reaches a certain point, the remaining nephrons begin a process of irreversible sclerosis that leads to a progressive decline in the GFR.

Staging:

Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2)

Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2)

Stage 3a: Moderate reduction in GFR (45-59 mL/min/1.73 m2)

Stage 3b: Moderate reduction in GFR (30-44 mL/min/1.73 m2)

Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2)

Stage 5: Kidney failure (GFR < 15 mL/min/1.73 m2 or dialysis).

Diagnosis:

By itself, measurement of GFR may not be sufficient for identifying stage 1 and stage 2 CKD, because in those patients the GFR may in fact be normal or borderline normal. In such cases, the presence of one or more of the following markers of kidney damage can establish the diagnosis.

Albuminuria (albumin excretion > 30 mg/24 hr or albumin:creatinine ratio > 30 mg/g [> 3 mg/mmol])

Urine sediment abnormalities

Electrolyte and other abnormalities due to tubular disorders

Histologic abnormalities

Structural abnormalities detected by imaging

History of kidney transplantation in such cases

Signs and symptoms:

Signs of alterations in the way the kidneys are handling salt and water in stage 5 include the following:

• Peripheral edema

• Pulmonary edema

• Hypertension.

Laboratory studies used in the diagnosis of CKD can include the following

• Complete blood count (CBC)

• Basic metabolic panel

• Urinalysis

• Serum albumin levels: Patients may have hypoalbuminemia due to malnutrition, urinary protein loss, or chronic inflammation

• Lipid profile: Patients with CKD have an increased risk of cardiovascular disease.

• Imaging studies also done accordingly.

Mangement:

Delaying or halting the progression of CKD: Treatment of the underlying condition, if possible, is indicated

Diagnosing and treating the pathologic manifestations of CKD

Timely planning for long-term renal replacement therapy

QUESTION 5

Testing scholarship competency in logging reflective observations on your concrete experiences of this last month

This month I had given chance to make an elog of CRF case and I came to know more clinical signs and symptoms related to the disease and also I came to understand some Pharmacological aspects of Prescription writing of main drug- adjuvant-and corrective drugs .And I had great learning experience more from this present assessment which had given chance to go through such interesting cases and good presenting and easy understanding e logs .

Thank you 

Soumya Menda 

Roll No. 80 

3 RD Semester .