October Internal Assesment

 JAHNAVI CHATLA

4TH YEAR MBBS

We have been assigned to elog our internal assessment questions where the goal is to achieve learning driven through searchable information, particularly with regard to making original contributions and avoiding plagiarism from the searched work.

Here is my attempt of doing so.

Our question paper has been prepared as to assess our ability in our clinical postings regarding " Patient clinical data analysis" to develop our competancy in comprehending clinical data including history, clinical finding, investigations and come up with a  diagnosis and treatment plan.

NOTE: All the questions in the below question paper had been some of cases in our medical college in this past month.

QUESTION 1

DEFINE BONE DENSITY, HOW IS IT MEASURED? WHAT ARE THE CAUSES, CLINICAL FEATURES, DIAGNOSIS AND MANAGEMENT OF OSTEOPOROSIS?

    

           

Extra points taken from the below link

https://en.m.wikipedia.org/wiki/Osteoporosis

BONE DENSITY:

The amount of bone mineral in bone tissue is called bone density

MEASURING BONE DENSITY

• Z score: the number of standard deviations above or below the mean for the patient's age, sex and ethnicity.
• T score: the number of standard deviations above or below the mean for a healthy 30-year-old adult of the same sex and ethnicity as the patient.

OSTEOPOROSIS 

Osteoporosis is defined as a bone density of 2.5 SD below that of a young adult. 

Osteoporosis is a systemic skeletal disorder characterized by low bine mass, micro-architectural deterioration of bone tissue leading to bone fragility, and consequent increase in fracture risk.

Causes:

Osteoporosis may also occur due to a number of diseases or treatments, including alcoholism, anorexia, hyperthyroidism, kidney disease, and surgical removal of the ovaries. Certain medications increase the rate of bone loss, including some antiseizure medications, chemotherapy, proton pump inhibitors, selective serotonin reuptake inhibitors, and glucocorticosteroids. Smoking, and too little exercise are also risk factors.

Pathogenesis 

The three main mechanisms by which osteoporosis develops are an inadequate peak bone mass (the skeleton develops insufficient mass and strength during growth), excessive bone resorption, and inadequate formation of new bone during remodeling, likely due to mesenchymal stem cells biasing away from the osteoblast and toward the marrow adipocyte lineage.

Diagnosis

Bio markers :Chemical biomarkers are a useful tool in detecting bone degradation. The enzyme cathepsin K breaks down type-I collagen, an important constituent in bones. Prepared antibodies can recognize the resulting fragment, called a neoepitope, as a way to diagnose osteoporosis. Increased urinary excretion of C-telopeptides, a type-I collagen breakdown product, also serves as a biomarker for osteoporosis.

2)DEFINE MYXOEDEMA COMA? DESCRIBE ITS CLINICAL FEATURES, DIAGNOSIS AND TREATMENT.

Extra points taken from the below link

https://en.m.wikipedia.org/wiki/Myxedema_coma

A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event (such as an infection, myocardial infarction, or stroke) precipitates the myxedema coma state, usually in the elderly.

Clinical feature

• Cardiovascular
  • Bradycardia
  • Bundle branch blocks
  • Complete heart block and arrhythmias
  • Cardiomegaly
  • Elevated diastolic blood pressure—early
  • Hypotension—late
  • Low cardiac output
  • Non-specific ECG findings
  • Pericardial effusion
  • Polymorphic ventricular tachycardia (torsades de pointes)
  • Prolonged QT interval
• Respiratory
  • Hypoxia
  • Hypercarbia
  • Hyperventilation
  • Myxedema of the larynx
  • Pleural effusion
• Gastrointestinal
  • Abdominal distention
  • Abdominal pain
  • Anasarca
  • Anorexia and nausea
  • Decreased motility
  • Fecal impaction and constipation
  • Gastric Atony
  • Myxedema or toxic megacolon—late
  • Neurogenic oropharyngeal dysphagia
  • Paralytic ileus
• Neurological
  • Altered mentation
  • Coma
  • Confusion and obtundation
  • Delayed tendon reflexes
  • Depression
  • Poor cognitive function
  • Psychosis
  • Seizures
• Renal and urinary function
  • Bladder dystonia and distension
  • Fluid retention
• Appearance and dermatological
  • Alopecia
  • Coarse, sparse hair
  • Dry, cool, doughy skin
  • Myxedematous face
  • Generalized swelling
  • Goiter
  • Macroglossia
  • Non-pitting edema
  • Ptosis
  • Periorbital edema
  • Surgical scar from prior thyroidectomy
• Hypothermia

Laboratory features in myxedema coma:^[

• Anemia
• Elevated creatine kinase (CPK)
• Elevated creatinine
• Elevated transaminases
• Hypercapnia
• Hypercholesterolemia (elevated LDL)
• Hyperlipidemia
• Hypoglycemia
• Hyponatremia
• Hypoxia

Physical findings in myxedema coma may include the classic myxedematous face, which is characterized by generalized puffiness, macroglossia, ptosis, periorbital edema, and coarse, sparse hair. Nonpitting edema of the lower extremities is sometimes present. The findings from a thyroid examination are usually normal, but a goiter may be present in some patients. The presence of a scar on the neck might suggest postsurgical hypothyroidism and may be an important clue in the diagnosis of a patient who is comatose. A neurologic examination may reveal decreased reflex tendon relaxation and will invariably reveal altered mentation.

3)WHAT IS THE DIAGNOSTIC APPROACH OF YOUNG ONSET HYPERTENSION AND ITS TREATMENT?

Early onset hypertension (<35 years )confers increased risk for cardiovascular mortality in the community. Hypertension onset at age <35 years of age was associated with significantly increased odds of LVH, coronary calcification, and left ventricular diastolic dysfunction in middle-aged individuals 

4)HOW DO YOU CLINICALLY LOCALISE THE ANATOMICAL LEVEL OF LESION IN SPINAL CORD DISEASES

It extends from Cranial border of atlas to L1 vertebrae( lower border)

It’s caudal end consists of Conus medullaris which contains S3 S4 S5 

SPINAL CORD LEAION LOCALISATION 

AT THE LEVEL

Motor- Segmental LMN finding

Sensory- Segmental sensory root findings

BELOW THE LEVEL

Motor - UMN finding

Sensory- Tract involvement findings

Automatic- Bladder and Bowel findings

INTRA MEDULLARY LESION

Dysesthesia, Paresthesia

Dissociated sensory loss

Sacral spacing is present

Spastic paralysis not prominent

Muscle atrophy common

Tropic skin changes common

Bladder and bowel disturbances occur early if lesion is lower

EXTRAMEDULLARY LOCALISATION 

Root pain

Segmental wasting

Spastic paralysis 

Bladder and bowel symptoms occur late

LOCALISATION AT CONUS

Bladder incontinence

Bowel incontinence

Loss of penile Tunescence

Loss of anal reflex 

Loss of Bulbocavernous reflex

Perinatal sensory loss

No motor weakness

5) CAUSES, DIAGNOSIS AND TREATMENT OF AYRIAL FIBRILLATION?

Symptomatic episodes may involve heart palpitations, fainting, lightheadedness, shortness of breath, or chest pain.Atrial fibrillation is associated with an increased risk of heart failure, dementia, and stroke.

High blood pressure and valvular heart disease are the most common modifiable risk factors for AF. Other heart-related risk factors include heart failure, coronary artery disease, cardiomyopathy, and congenital heart disease. In the low- and middle-income countries, valvular heart disease is often attributable to rheumatic fever.Lung-related risk factors include COPD, obesity, and sleep apnea.Other risk factors include excess alcohol intake, tobacco smoking, diabetes mellitus, and thyrotoxicosis.

6)DESCRIBE ABOUT MEGALOBLASTIC ANEMIA 

Megaloblastic anemia is a type of macrocytic anemia. An anemia is a red blood cell defect that can lead to an undersupply of oxygen. Megaloblastic anemia results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis

7)WHAT ARE THE CAUSES PATHOGENESIS AND DDs OF ASCITES?

 

Ascites exists in three grades:
Grade 1: mild, only visible on ultrasound and CT
Grade 2: detectable with flank bulging and shifting dullness
Grade 3: directly visible, confirmed with the fluid wave/thrill test

8)APPROACH TO ACUTE PANCREATITIS 

Causes in order of frequency include: 1) a gallstone impacted in the common bile duct beyond the point where the pancreatic duct joins it; 2) heavy alcohol use; 3) systemic disease; 4) trauma; 5) and, in minors, mumps. 

9)MENTION THE DIFFERENCE BETWEEN UMN AND LMN LESION?

10)INDICATIONS OF HEMODIALYSIS 

Indications of dialysis in acute renal failure (ARF)

• Severe fluid overload
• Refractory hypertension
• Uncontrollable hyperkalemia
• Nausea, vomiting, poor appetite, gastritis with hemorrhage
• Lethargy, malaise, somnolence, stupor, coma, delirium, asterixis, tremor, seizures,
• Pericarditis (risk of hemorrhage or tamponade)
• bleeding diathesis (epistaxis, gastrointestinal (GI) bleeding and etc.)
• Severe metabolic acidosis
• Blood urea nitrogen (BUN) > 70–100 mg/dl

Indications of dialysis in chronic renal failure (CRF)

• Pericarditis
• Fluid overload or pulmonary edema refractory to diuretics
• Accelerated hypertension poorly responsive to antihypertensives
• Progressive uremic encephalopathy or neuropathy such as confusion, asterixis, myoclonus, wrist or foot drop, seizures
• Bleeding diathesis attributable to uremia

11) WHAT IS THE ROLE OF SUCRALFATE

Sucralfate, a basic aluminum salt of sucrose, was the first successful drug with a major cytoprotective mechanism of action. It binds bile acids and pepsin and adheres to both ulcerated and nonulcerated mucosa. Sucralfate stimulates the synthesis and release of gastric mucosal prostaglandins as well as bicarbonate and the epidermal growth factor which stimulates healing.

12)RENAL MANIFESTATIONS OF SNAKE BITE

Mesangiolysis, glomerulonephritis, vasculitis, tubular necrosis, interstitial nephritis and cortical necrosis. Tubular necrosis is an important pathological counterpart of acute renal failure. 

13)CAUSES OF PORTAL HYPERTENSION 

Prehepatic

EHPVO

Congenital stenosis of portal vein

External compression of portal vein

Arterio portal fistula

Hepatic

Cirrhosis 

Congenital hepatic fibrosis 

Hepatic portal sclerosis 

Nodular regenerative hyperplasia

Venoocclusive disease 

Granulomatous disease

Post hepatic

Hepatic vein thrombosis 

Congenital malformations and thrombosis of IVC

Constrictive pericarditis 

14)DOWN’S SYNDROME

15)Renal manifestations of PSGN

16)CAUSES OF CERVICAL MYELOPATHY