Bimonthly blended assessment - June 2021 July 03, 2021

NAME:KAVYA SREE KALUVALA 
ROLL NO:04(OLD BATCH)
BATCH:3RD SEMISTER

             I have been given the following cases to solve in an attempt to understand the topic of 'patient clinical data analysis 'to develop my competency in reading and comprehending clinical data including history ,clinical findings, investigation and diagnosis and come up with the treatment plan.

This is the link of questions asked regarding the cases:

http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

Below are my answers to the medicine assignment based on my comprehension of the cases.

QUESTION:1

PULMONOLOGY:

        CASE:1

1)A 55-year-old female with shortness of breath ,pedal Edema ,and facial puffiness

Below are my answers to the medicine assignment based on my comprehension of the cases.

The Patient came to the hospital with the chief complaints of shortness of breath, pedal edema, facial puffiness, decreased urine output, drowsiness and chest pain. After all required investigations she diagnosed as exacerbation of COPD associated with right heart failure and bronchiectasis. Diuretics, Steroids and antibiotics are used for treating the symptoms. The case was explained well and treatment for all the symptoms was given properly.
  • he anatomical localization of the problem is at the bronchioles.
  • etiology-its is due exposue of dust /allergens in paddy feilds


NEUROLOGY:


 NEUROLOGY 

CASE 1

1) A 40 year old male with complains of irrelevant talking.


a)

  • anatomical location and pathophysiology
         *  Ethanol is a central nervous system depressant that produces euphoria and behavioral excitation at low blood concentrations due to increased glutamate binding to N-methyl-D-aspartate (NMDA) receptors; at higher concentrations, it leads to acute intoxication by potentiation of the gamma-aminobutyric acid (GABA) effects, particularly in receptors with delta subunits. The local distribution of these subunits explains why the cerebellum, cortical areas, thalamic relay circuitry, and brainstem are the main networks that mediate the intoxicating effects of alcohol.

*Prolonged alcohol use leads to the development of tolerance and physical dependence, which may result from compensatory functional changes by downregulation of GABA receptors and increased expression of NMDA receptors with production of more glutamate to maintain central nervous system (CNS) transmitter homeostasis

*Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate-mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures.The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits.



b)

 1. IVF NS and RL 

 mechanism:Administer intravenous (IV) fluids for rehydration, as necessary. Most patients with severe alcohol withdrawal are significantly dehydrated, and their fluid requirements range from 4-10 L in the first 24 hours. Because hypoglycemia is common in these patients due to depleted glycogen stores, a 5% dextrose solution (in 0.90% or 0.45% saline) should be used to prevent hypoglycemia.

2. Inj. THIAMINE 
mechanism:
*
  • It is well known that chronic alcoholics are at high risk for being deficient in vitamin B1 (thiamine), which is known to put the patient at an increased risk for Wernicke-Korsakoff Syndrome, cerebellar degeneration, and cardiovascular dysfunction.
  • What does thiamine contribute that allows the cells in the brain to respond to this metabolic demand?
    Upon absorption into the body, thiamine is used to form thiamine pyrophosphate, which is an essential co-factor used by several cellular enzymes.


3. Inj. Lorazepam
mechanism:Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell.

4. T. Pregabalin 
mechanism: Pregabalin is structurally related to the antiepileptic drug gabapentin and the site of action of both drugs is similar, the alpha2-delta (alpha2-delta) protein, an auxiliary subunit of voltage-gated calcium channels. Pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions in vivo to reduce neuronal excitability and seizures.

5. Inj. HAI S.C.- premeal
mechanism:Regulates glucose metabolism

Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue

6. GRBS 
mechanism:Regular blood glucose monitoring is an essential tool to help you take control of your diabetes. By identifying and recording changes in your blood sugar levels, you'll have more information about how food, exercise, stress, and other factors affect your diabetes.

7. glucose monitoring
mechansm:Regular blood glucose monitoring is an essential tool to help you take control of your diabetes. By identifying and recording changes in your blood sugar levels, you'll have more information about how food, exercise, stress, and other factors affect your diabetes.

8. Inj  ampoule KCl 
mechanism:Potassium ions participate in a number of essential physiological processes, including the maintenance of intracellular tonicity; the transmission of nerve impulses; the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of normal renal function.

9. Syp Potchlor 
mechanism:It helps to maintain potassium balance in the body by restoring normal potassium levels in patients with a low level of potassium

c)
Long-term abuse can damage the nervous system liver and other organs this damage maybe is reversible drinking too much alcohol can also alter the level of certain nutrients in the body including
* thiamine
* folate
* vitamin B6 and B 12
vitamins are needed for proper no function and can also cause alcohol related neurological diseases.

d)

 thiamine is used to form thiamine pyrophosphate, which is an essential co-factor used by several cellular enzymes.3  The pyrophosphate portion added to thiamine is important since this group is used to bind to magnesium and then further bind to amino acid side chains on the cellular enzyme.3  This allows the thiamin pyrophosphate to function as a co-factor to that enzyme so that it can facilitate the forward movement of its assigned biochemical reactions.  One of the most important sets of biochemical reactions requiring the availability of thiamine includes the reactions involved in glycolysis and the tricarboxylic acid (TCA) cycle.  There are three enzymes that facilitate several reactions involved in these processes that require the presence of thiamine pyrophosphate.  These enzymes are a-ketoglutarate dehydrogenase, branched chain amino acid dehydrogenase, and pyruvate dehydrogenase. The forward movement of glycolysis and the TCA cycle are essential for the cell's ability to generate the ATP needed to maintain other cellular activity. 

e)

The sudden removal of alcohol can also cause kidney failure. Alcohol has to be broken down and cleared from the body as urine. This needs water, as the products of the breakdown have to be in solution.

Alcohol also inhibits the production of an anti-diuretic hormone, so large quantities of alcohol make you urinate a lot and become dehydrated. Electrolytes in the body, such as sodium, magnesium, calcium and potassium, are usually in solution (water) and excessive amounts of alcohol can cause an imbalance in these electrolytes as well as an acid-base imbalance. These imbalances can eventually lead to acute kidney failure.

f)

the affected kidney leads to

1) a moderately reduced red cell life span,

 2) blood loss, and 

3) an inadequate increase in erythropoiesis relative to the fall in hemoglobin (Hb).


g) 
excessive alcohol can cause nutritional deficiency and alcohol toxicity these in turn can cause poor nutrition leading to poor wound healing and problems with nerves (neuropathy) when sensory nerves in the foot stops working the foot can get injured and this leads to foot


CARDIOLOGY:


CASE1


A-Fib and Biatrial Thrombus in a 52yr old Male



a)

*the anatomical site is BLOOD VESSELS;
* ETIOLOGY: 
The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.

b)PHARMACOLOGICAL INTERVENTIONS

1. TAB. Dytor

mechanismThrough its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.

2. TAB. Acitrom 

mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting

3. TAB. Cardivas 

mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.


4. INJ. HAI S/C

MECHANISM:Regulates glucose metabolism

Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue

5.TAB. Digoxin 

mechanism:

Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:

 Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,

 an enzyme that controls the movement of ions into the heart.

6. Hypoglycemia symptoms explained

7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.

8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.


c)



*cardiorenal syndrome type 4 is seen in this patient.


d)
effect of hypertention
 They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.



e)

APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.

 4.Gastroenterology:



                  The Patient came to the hospital with the chief complaints of pain abdomen, Vomting since 1 week, Constipation, Burning Micturition and fever since 4 days. After all investigations he diagnosed as acute on chronic pancreatitis with pseudocyst and acute infective peri pancreatic fluid collections, moderate left pleural effusion with basal atelectasis, left pneumothorax, secondary to broncho pleural fistula. The presentation was clear and well explained

5. Nephrology (and Urology): 



                   The Patient came to the hospital with the chief complaints of fever since 4 days, pus in the urine. previously he presented with multiple complaints like drowsiness, excessive sleep, burning micturition, suprapubic pain and dribbling urine. prostamegaly was seen. After all the investigations he diagnosed as Renal AKI secondary to urosepsis with b/L hydroureteronephrosis with K/c/of DM -2 since 5 yrs with diabetic nephropathy with Anemia secondary to CKD with grade 1 bed sore. Treatment for all the symptoms was given.

6. Infectious Diseases(HI virus, Mycobacteria, Gastroenterology,pulmonogy): 




                    The Patient came to the hospital with the chief complaints of difficuilty in swallowing, fever and cough since 2 months. Weight loss of 10kgs, Hoarseness of voice, inadequate sleep since 2 months. After all examination and investigations she diagnosed 
14/05/2021:
40/female with RVD since 2 months on ART with dysphagia secondary to Esophageal Candidiasis ?Tracheoesophageal fistula ? Stricture 
It can be any of the above diagnosis
22/05/2021:
40/female with RVD with DISSEMINATED TB with TEF 2° to ? TV/MALIGNANCY with ANAPHYLAXIS 2° to radio contrast (resolving).
                   Presentation was well explained.

7. Infectious Diseases and Hepatology:


                   
                    The patient came to the hospital with the chief complaints of pain abdomen since 1week,decrease appetite since 1week ,fever since 4 days.He is chronic alcoholic since 30 yrs.
After all the investigations, systemic examination he diagnosed as liver abscess.The symptoms were treated and adviised medications on discharge and weekly follow up

8. Neurology: 


                    
                   The patient came to the hospital with the chief complaints of slurring speech ,deviation of mouth. He has postural instability, vomiting. After all systemic examination and investigations he diagnosed as cerebellar ataxia secondary to acute cerebrovascular accident (CVA) with infract in the right inferior cerebellar hemisphere. the presentation was accurate and clear.

9. Cardiology:



                     The patient came to the hospital with the chief complaints of shortness of breath since 1/2 hr.she has TB diagnosed 7 months ago. After all investigations she diagnosed as acute coronary syndrome (NSTEM).The patient was then advised to shift to a HC for PCI,but pci was not done bcz of no vacancy.she shifted to another hospital for further treatment.The presentation was good.

10. Infectious     disease(Mucormycosis,Ophthalmology,Otorhlnolaryngolo               gy,Neurology):


                 The patient came to the hospital with the chief complaints of fever since 10 days ,fascial puffiness,periorbital edema since 4 days,weakness of right upper limb and lower limb since 4 days,altered sensorium since 2 days.day1 evng serious discharge from left eye. After all investigations he diagnosed as ACUTE ORO RHINO ORBITAL MUCORMYCOSIS WITH DIABETIC KETO ACIDOSIS WITH RIGHT SIDED CVA  (ACUTE INFARCT IN LEFT FRONTAL AND TEMPORAL LOBE) WITH DENOVO DETECTED DIABETES MELLITUS 2 WITH AKI AND HYPERTENSION SINCE 2 YEARS. the explaination was very well,treatment for the symptoms was given,presentation was clear


Question No-2:
       I haven't got the chance.

Question No-3:


         The patient presented to casuality with complaints of sudden fall followed by weakness of both the lower limbs (paraplegia) and loss of hand grip, associated with bowel and bladder incontinence.He developed generalised weakness and myalgia,cough,low grade fever which he under went sputum studies and tested positive for AFB bacilli and started ATT-HRZE regimen,2 tab according to weight/PO/OD.He is a known case of TB since 1 month. After all the investigations he diagnosed as quadreparesis secondary to infectious spondylitis of C4,C5,C6,C7,and D1 with Epidural abscess at C5-C6 level

Question No-4:


            The patient with chief complaints of abdominal distension and shortness of breath.Hypothyroidism since 5 yrs .she was thyronom100mg OD for hypothyroidism.After all ivestigations she diagnosed as HFrEF with Atrial fibrillation 2to ? IHD.Her biochemical report showing severe hpothyroidism possibly relating to her refractory atrial fribrillation ad attempted for defribrillation.she had low bp .There is no mention of thyroid test reports ,may be performing thyroid test earlier could have been liife saving.

Question No-5:

              Last month we just began our clinical postings through online.
First time it is very difficult for us ,but with this blogs we are atleast knowing the basic things like history taking etc.
Due do this pandemic our learing became very tough because everything is online.
 Our Professors ,PGS ,Interns helping us to learn subject through blogs .
 We are unable to attend offline postings, in this situation eblogs are very helpful as we are taking up a case.
Our HOD of general medicine exaplaining each and every case.
 Thank you general medicine department for this eblog idea and helping us to learn.

THANK YOU-

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