OPINION OF CASES BY 172

 

NEUROLOGY

 

Case A:  

 

A 40 year old male presented to the hospital from Yadagirigutta with the chief complaints of irrelevant talking and decreased food intake since 9 days. 

 

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

 

Questions:

 

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

EVOLUTION OF SYMPTOMATOLOGY:

12 YEARS AGO

·        Addicted to alcohol, drinks about 3-4 quarters per day

2 YEARS AGO

·        Diagnosed with type 2 Diabetes (irregular medication; once in 2 or 3 days)

1 YEAR AGO

·        1-2 episodes of seizures (mostly due to alcohol consumption)

4 MONTHS AGO

·        Developed a seizure (mostly GTCS)

·        Cessation of alcohol for 24 hours assosiated with symptoms of restlessness, sweating, and tremors.

10 DAYS AGO

·        General body pains

9 DAYS AGO

·        Started talking and laughing to himself (sudden onset)

·        Decreased food intake

·        Required assistance to move around

·        Short term memory loss (couldn't recognise family members)

·         

 

 

 

ANATOMICAL LOCALISATION

 

 

PRIMARY ETIOLOGY

·        Wernicke's encephalopathy: thiamine deficiency secondary to alcohol dependence

·        Uremic encephalopathy: 

·        Altered sensorium: alcohol withdrawal syndrome

 

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

1) Drug name: SYP POTKLOR 

 

MOA: It inceases the potassium levels

 

Indication: This medicine is used for the prevention or treatment of low potassium levels in the blood (Hypokalemia).

 

 

2)Drug name: PREGABALIN

 

MOA: Although the mechanism of action has not been fully elucidated, studies involving structurally related drugs suggest that presynaptic binding of pregabalin to voltage-gated calcium channels is key to the antiseizure and antinociceptive effects observed in animal models.

 

Indication: Pregabalin is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain associated with spinal cord injury, and as adjunctive therapy for the treatment of partial-onset seizures

 

Efficacy over Pregabalin:

·        P : 539

·        I : pregabalin

·        C : 265

·        O :  the most common adverse events were dizziness and somnolence 

https://go.drugbank.com/drugs/DB00230 

https://pubmed.ncbi.nlm.nih.gov/30242745/

 

 

3) Drug name: KCl

 

MOA: For use as an electrolyte replenisher and in the treatment of hypokalemia.

 

Indication: For use as an electrolyte replenisher and in the treatment of hypokalemia.

 

Efficacy over KCL:

·        p : 18

·        i : KCl

·        c : random number of patients

·        o : amiloride might be more effective than potassium chloride in preventing hypokalaemia

https://go.drugbank.com/drugs/DB00761

https://pubmed.ncbi.nlm.nih.gov/3911735/

 

·        INJ NS and RL : Lactated Ringer's is a sterile, nonpyrogenic solution for fluid and electrolyte replenishment and caloric supply in a single dose container for intravenous administration.

https://www.rxlist.com/lactated-ringers-in-5-dextrose-drug.htm

 

4) Drug name:  LORAZEPAM

 

MOA: Lorazepam allosterically binds on the benzodiazepine receptors in the post-synaptic GABA-A ligand-gated chloride channel in different sites of the central nervous system (CNS). This binding will result in an increase on the GABA inhibitory effects which is translated as an increase in the flow of chloride ions into the cell causing hyperpolarization and stabilization of the cellular plasma membrane.

 

Indication: Lorazepam is FDA-approved for the short-term relief of anxiety symptoms related to anxiety disorders and anxiety associated with depressive symptoms such as anxiety-associated insomnia. It is as well used as an anesthesia premedication in adults to relieve anxiety or to produce sedation/amnesia and for the treatment of status epilepticus.

 

Efficacy over lorazepam:

·        P : 56

·        I : lorazepam

·        C : 21

·        O : The effect size achieved in the placebo group was not inferior to that of benzodiazepines in general.

https://go.drugbank.com/drugs/DB00186

https://pubmed.ncbi.nlm.nih.gov/2575766/

 

 

 

3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

 

Patient had increased symptoms because he relapsed and drank alcohol again. Usually if you stop taking alcohol and start again patient will have severe withdrawal symtoms next time whenn he stops.

 

 

4) What is the reason for giving thiamine in this patient?

 

 Wernicke’s encephalopathy is an acute neuropsychiatric disorder that occurs as a result of thiamine (vitamin B1) deficiency. Thiamine has been administered to counteract its deficiency.

 

 

5) What is the probable reason for kidney injury in this patient? 

 

Chronic alcohol consumption might have lead to kidney injury in this patient.

 

 

 

6). What is the probable cause for the normocytic anemia?

 

The most common cause of normocytic anemia is a long-term (chronic) disease. In this case, the patient has been suffering from uremic encephalopathy which is an organic brain disorder. It develops in patients with acute or chronic renal failure, usually when the estimated glomerular filtration rate falls and remains below 15 mL/min.

 

7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

 

Yes, excessive alcohol can cause nutritional deficiencies and alcohol toxicity. These in turn can cause poor nutrition leading topoor wound healing and problems with nerves. When the sensory nerves in the foot stop working, the foot can get injured and this leads to food ulcers.

 

 

 

 

Case B:

 

A 52 year old male came to the hospital 2 days back presenting with slurring of speech and deviation of mouth that lasted for 1 day and resolved on the same day. 

 

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

 

Questions:

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

EVOLUTION OF SYMPTOMATOLOGY

7 DAYS AGO

·        Giddiness assosiated with an episode of vomiting

3 DAYS AGO

·        Giddiness - sudden in onset                                                                                                                                     - continuous and gradually progressive                                                                                                   -increased in severity upon getting up from the bed and while walking                                                 -associated with bilateral Hearing loss, aural fullness and presence of tinnitus              

·        Vomiting (2-3 episodes per day), non projectile, non bilious containing food particles                      

·        Postural instability

 

ANATOMICAL LOCALISATION

 

 

 

ETIOLOGY OF DISEASE IN PATIENT

 

 

 

 

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

 

 

 

 

 

 

3) Did the patients history of denovo HTN contribute to his current condition?

 

The patients history of denovo HTN might have been contributed to his current condition as, long history and irregular medication can lead to peripheral neuropathy which in this case might have lead to cerebral atresia.

 

 

4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?

 

Alcohol may increase the risk of hemorrhagic stroke. It is caused by a blood clot blocking the flow of blood and oxygen from reaching the brain.

 

 

 

 

 

Case C:

 

A 45 years old female ,house wife by occupation came to opd with chief complaints of palpitations, chest heaviness, pedal edema, chest pain, radiating pain along her left upper limb.

 

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Questions:

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

EVOLUTION OF SYMPTOMATOLOGY

10 YEARS AGO

·        Paralysis of both upper and lower limbs (right and left)

1 YEAR AGO

·        Right and left paresis due to hypokalemia

8 MONTHS AGO

·        Bilateral pedal edema - gradually progressing                                                                                                                            - present both in sitting and standing position                                                                                        - relieved on taking medication

·        Swelling over the legs (bilateral)

7 MONTHS AGO

·        Blood infection

2 MONTHS AGO

·        Treatment of neck pain

6 DAYS AGO

·        Pain - radiating along the the left upper limb                                                                                                  - dragging in nature, aggrevated during palpitations                                                                              - relieved by taking medication for palpitations

·        Chest pain associated with chest heaviness

5 DAYS AGO

·        Could feel her own heartbeat

·        Chestpain

·        Difficulty in breathing

·        Palpitations - since sudden in onset, more during night time                                                                                   

·          - aggregated by lifting weights, speaking continuously                                                                         

·         - it is relieved by drinking more water and medication

·        Dyspnoea during palpitations (NHYA-CLASS-3)

 

ANATOMICAL LOCALISATION

·        Neural system due to hypokalemia

 

PRIMARY ETIOLOGY

·        Most probably due to the electrolyte imbalances.

 

 

2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

 

Reason for recurrence of hypokalemia in this patient is due to recurrent hypokalemic periodic paralysis. The current risk factor is mainly due to administration of diuretics. Other risk factors are:

 

a) Abnormal loses due to medications, osmotic diuresis, renal tubular acidosis, hypomagnesemia.

b) Trance cellular shifts

c) Inadequate intake

d) Pseudohypokalemia

 

 

 

3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?

 

ECG changes include:

·        Flattening and inversion of T waves in mild hypokalemia

·        Q-T interval prolongation

·        Visible U wave and mild ST depression in more severe hypokalemia

·        Severe hypokalemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.

Clinical symptoms of hypokalemia do not become evident until the serum potassium level is less than 3 mmol/L. The severity of symptoms also tends to be proportional to the degree and duration of hypokalemia. 

 

The assosiated symptoms are:

·        Muscle weakness (the pattern is ascending in nature affecting the lower extremities, progressing to involve the trunk and upper extremities and potentially advancing to paralysis).

·        Fatigue

·        Constipation

·        Muscle twitches

·        Palpitations

In more severe cases, abnormal rythms may occurs:

·        Atrial or ventricular fibrillation

·        Premature heartbeats

·        Tachycardia

·        Bradycardia

 

 

 

 

 

Case D:

 

A 55year old male patient came to OPD with c/o altered sensorium and involuntary movements from 11pm and recurrent episodes of seizures since 5yrs.

 

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

 

Questions:

 

1) Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

 

Yes, post‐stroke seizure and post‐stroke epilepsy are common causes of hospital admissions, either as a presenting feature or as a complication after a stroke. Also taking into consideration the age of our patient, it is to be noted that stroke is the most common cause of seizures in the elderly population.

 

Causes for early onset seizures after ischaemic strokes:

·        An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation

·         Glutamate excitotoxicity

·         Hypoxia

·         Metabolic dysfunction

·         Global hypoperfusion

·         Hyperperfusion injury.

Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring. Haemosiderin deposits are thought to cause irritability after a haemorrhagic stroke.

 

 

 

2) In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

 

The patient might have experienced a grand mal seizure — also known as a generalized tonic-clonic seizure in his last episode.  It is defined as a seizure that has a tonic phase followed by clonic muscle contractions. They are usually associated with impaired awareness or complete loss of consciousness.

 

 

 

 

 

Case E:

 

A 48-year-old gentleman hailing from a small town in Telangana presented to the casualty ward on 25th April 2021 at 7:40am with the chief complaints of unresponsiveness for 7 hours and 3 intermittent episodes of seizures in the past 3 hours.

 

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

 

Questions:

 

1) What could have been the reason for this patient to develop ataxia in the past 1 year?

 

 Ataxia usually results from damage to a part of the brain called the cerebellum, but it can also be caused by damage to other parts of the nervous system. 

 

This damage can be caused by 

·        a head injury

·        lack of oxygen

·         long-term consumption of alcohol.

·        underlying conditions such as MS

 As the patient has a h/o minor head injuries and addiction to alcohol since 3 years, he might've developed ataxia.

 

2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?

 

The probable reasons for IC bleed in this case are:

·        Chronic alcohol abuse assosiated to high blood pressure which can cause the thin-walled arteries which supply blood to the brain to rupture, releasing blood into the brain tissue.

·        Untreated head injuries                                                                                    

Assosiation of alcohol with bleeding disorders:

·        Alcohol has numerous adverse effects on the various types of blood cells and their functions. Heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that cannot mature into functional cells.

·         Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. 

·        Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria.

·         Consequently, alcoholics frequently suffer from bacterial infections. Finally, alcohol adversely affects the platelets and other components of the blood-clotting system. Heavy alcohol consumption thus may increase the drinker's risk of suffering a stroke.

 

 

 

 

Case F:

 

A 30 year old male patient lorry driver by occupation came to the OPD with chief complaints of weakness of right upper and lower limb since one day and deviation of mouth towards left since one day.

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Questions:

1. Does the patient's  history of road traffic accident have any role in his present condition?

No.

2. What are warning signs of CVA?

·        Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.

·        Sudden confusion, trouble speaking, or difficulty understanding speech.

·        Sudden trouble seeing in one or both eyes.

·        Sudden trouble walking, dizziness, loss of balance, or lack of coordination.

·        Sudden severe headache with no known cause.

3.What is the drug rationale in CVA?

·        Drug treatment of CVA involves intravenous thrombolysis with alteplase. Intravenous alteplase promotes thrombolysis by hydrolyzing plasminogen to form the proteolytic enzyme plasmin. Plasmin targets the blood clot with limited systemic thrombolytic effects.

·         Other acute supportive interventions for CVA include maintaining normoglycemia, euthermia and treating severe hypertension. 

·        Urgent antiplatelet use for AIS has limited benefits and should only promptly be initiated if alteplase was not administered, or after 24 hours if alteplase was administered.

 

4. Does alcohol has any role in his attack?

 

Liver damage in chronic alcoholics can stop the liver from making substances that help blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.

 

5.Does his lipid profile has any role for his attack?

 

No.

 

 

 

 

Case G:

 

50-year-old male patient presented to hospital with complaints of weakness of all four limbs since 8 PM yesterday.

 

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

 

Questions:

 

1) What is myelopathy hand ?

 

A characteristic dysfunction of the hand in cervical spinal disorders with loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers.  It appears to be due to pyramidal tract involvement.

 

 

2) What is finger escape ?

 

It refers to the slightly greater abduction of the fifth digit, due to paralysis of the abducting palmar interosseous muscle and unopposed action of the radial innervated extensor muscles.

 

 

3) What is Hoffman’s reflex?

 

Hoffmann's reflex is a neurological examination finding elicited by a reflex test which can help verify the presence or absence of issues arising from the corticospinal tract. 

 

 

 

 

Case H:

 

A 17 year old female student by occupation presented to causality on 1/5/2021 with chief complaints of involuntary movements of both upper and lower limbs a day before.

 

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1         

 

 

Questions:

 

1) What can be  the cause of her condition ?  

 

 

2) What are the risk factors for cortical vein thrombosis?

·         

·        Risk factors for children and infants include:

·        Beta-thalassemia major

·        Heart disease — either congenital (you're born with it) or acquired (you develop it)

·        Iron deficiency

·        Certain infections

·        Dehydration

·        Head injury

·        Sickle cell anemia

·        For newborns, a mother who had certain infections or a history of infertility

      Risk factors for adults include:

·        Pregnancy and the first few weeks after delivery

·        Problems with blood clotting

·        Collagen vascular diseases

·        Obesity

·        Cancer

·        Inflammatory bowel disease like Crohn's 

·        Low blood pressure in the brain

·      

3)There was seizure free period in between but again sudden episode of GTCS, why? Resolved spontaneously, why?   

 

3 days after seizure free period  patient was tapered off Midazolam, phenobarbitone. ThIs might be the cause of GTCS.

 

4) What drug was used in suspicion of cortical venous sinus thrombosis?

 

Clexane 0.4ml/sc was started in suspicion of CSVT

 

 

 

 

 

 

 

GASTROENTROLOGY 

 

 

Case A:

 

A 33 yr old male daily wage labour worker from miryalaguda who is a chronic alcoholic and smoker came to hospital on 30/04/2021 with cheif complaints with of pain abdomen & vomiting since 1 week and constipation, burning micturition, fever since 4 days.

 

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

 

 

Questions:

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

EVOLUTION OF SYMPTOMATOLOGY

5 YEARS AGO

·        Pain in abdomen  

·        Vomiting  

(subsided by conservatibe treatment and abstinence of alcohol)

 

ONE YEAR AGO

·        Pain in abdomen and vomiting: 5-6 episodes

(resumed frequent intake of alcohol; conservative treatment by local RMP)

 

ONE WEEK AGO

·        Abdominal pain- 1) in umbilical, left hypochondriac, left lumbar and hypogastric region                                                2) throbbing type and radiating to back                                                                                                  3) assosiated with nausea and vomiting

·        Vomiting (one episode) - non bilious, non projectile, contains food particles and water

  4 DAYS AGO

·        Fever 

·        Constipation

·        Burning micturition                

DURING HOSPITAL STAY

·        Developed progressive pneumothorax

 

  ANATOMICAL LOCALISATION

1.      PANCREAS- a) Acute on chronic pancreatitis                                                                                                               b) Acute infective peri pancreatic fluid collections

2.      LESSER SAC- a) Pseudocyst

3.      LEFT LUNG- a) Moderate left pleural effusion with basal atelectasis

 

  ETIOLOGY OF DISEASE IN PATIENT

·        The main cause of pancreatitis in this patient is attributed to the chronic intake of alcohol.

·        Recurrent episodes of pancreatitis has to lead to various complications of pseudocyst formation in lesser sac due to pancreatic duct rupture and BRONCHO PLEURAL FISTULA leading to pneumothorax.

 

2) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

 

 

Octreotide:

The results of clinical investigations using somatostatin or its analogue are controversial, since all these trials had low statistical power. In a recent multicenter randomized controlled study with a large number of patients, no benefit of octreotide on progression or outcome was found. Chronic pancreatitis is characterized by an irreversible destruction of the exocrine and endocrine pancreatic parenchyma leading to maldigestion and diabetes. Pain, which may be caused by increased ductal pressure, is one of the most dominant symptoms in chronic pancreatitis. However, no beneficial effects on pain with pancreatic exocrine secretion-inhibiting drugs have been demonstrated. Treatment of other complications of the disease (pseudocyst formation, fistula and pancreatic ascites), with somatostatin or octreotide has given conflicting results. However, in a prophylactic clinical setting (e.g. elective pancreatic surgery) the inhibition of exocrine pancreatic secretion reduces complications.

 

A clinical and therapeutical study of 47 patients with the diagnosis of acute pancreatitis is reported. According to Ranson's criteria patients were initially classified as suffering from mild (28) and severe (18) acute pancreatitis. Twenty-eight, 11, 7 and 1 patients had biliary, alcoholic, idiopathic and neoplastic causes, respectively, of their conditions. The classification of episodes was made on the basis of clinical manifestations, biologic investigations, and imaging diagnosis, and is shown in the corresponding tables. The therapeutic profile was a randomized double-blind study: perfused somatostatin (SS) versus placebo (P) (physiologic saline 0.9%). The administration of somatostatin in perfusion (250 mcg/h/48 hours) did not improve significantly the parameters used to score the severity, although the mortality rate decreased significantly (p < 0.05) in the group of patients with the severe form of the disease.

 

Antibiotics:

The mortality rates were 5.26% (5/95) and 18.18% (16/88) in prophylactic antibiotics and placebo/none-treatment groups, respectively.

Material and methods: Seventy-three patients with severe pancreatitis were included in a prospective, randomized, clinical study in seven Norwegian hospitals. The number of patients was limited to 73 because of slow patient accrual. Severe pancreatitis was defined as a C-reactive protein (CRP) level of >120 mg/l after 24 h or CRP >200 48 h after the start of symptoms. The patients were randomized to either early antibiotic treatment (imipenem 0.5 g x 3 for 5-7 days) (imipenem group) (n=36) or no antibiotics (control group) (n=37).

 

Results: The groups were similar in age, cause of pancreatitis, duration of symptoms and APACHE II score. Patients in the imipenem group experienced lower rates of complications (12 versus 22 patients) (p=0.035) and infections (5 versus 16 patients) (p=0.009) than those in the control group. There was no difference in length of hospital stay (18 versus 22 days), need of intensive care (8 versus 7 patients), need of acute interventions (10 versus 13), nor for surgery (3 versus 3) or 30-day mortality rates (3 versus 4).

 

Conclusions: The study, although underpowered, supports the use of early prophylactic treatment with imipenem in order to

 

https://pubmed.ncbi.nlm.nih.gov/17506001/

 

TPN

The aim of the study was to evaluate and control the therapeutic validity of Somatostatin administration and the clinical benefits of parenteral nutrition during acute pancreatitis. We selected 31 patients with 1st and 2nd degree pancreatitis according to Ranson's classification. Diagnosis was based on clinical and humoral data and confirmed by echography and CT examinations. The most common etiological cause was biliary++ lithiasis (74.2%). All the patients in the study were split into two groups and received conventional treatment. The therapeutic schedule administered to group 1 included somatostatin (250 micrograms/h for 72-96 h), while group 2 received total parenteral nutrition with 2,000-2,500 Kal/day trough a central vein. The data obtained from our study demonstrated that both somatostatin and parenteral nutrition are valid tools during the acute phase of the disease. It must be pointed out that the former significantly influences the clinical course and allows a precise control of the painful symptomatology, the objective picture and the curve of the main hematochemical parameters. Parenteral nutrition betters the anabolic response of the organism during the acute phase and carries out an indirect antienzymatic response, so favouring a quicker recovery than observed in the group treated with somatostatin.

https://pubmed.ncbi.nlm.nih.gov/2566958/

 

USG drain

 

A single-center retrospective study was performed after obtaining Institutional review board approval for analyzing hospital records of patients with acute necrotizing pancreatitis from January 2012 to July 2017. Seventy-eight consecutive patients with necrotizing pancreatitis and acute necrotic collections (ANC) were managed with percutaneous catheter drainage (PCD) and catheter-directed necrosectomy, in early phase of the disease (< 21 days). Clinical data and laboratory parameters of the included patients were evaluated until discharge from hospital, or mortality.

 

Results

Overall survival rate was 73.1%. Forty-two (53.8%) patients survived with PCD alone, while the remaining 15 (19.2%) survivors needed additional necrosectomy. The timing of intervention from the start of the hospitalization to drainage was 14.3 ± 2.4 days. Significant risk factors for mortality were the presence of organ system failure, need for mechanical ventilation, renal replacement therapy, and the acute physiology and chronic health evaluation II (APACHE II) score. An APACHE II score cutoff value of 15 was a significant discriminant for predicting survival with catheter-directed necrosectomy.

 

Conclusion

An early PCD of ANC in clinically deteriorating patients with acute necrotizing pancreatitis, along with aggressive catheter-directed necrosectomy can avoid surgical interventions, and improve outcome in a significant proportion of patients with acute necrotizing pancreatitis.

https://link.springer.com/article/10.1007/s12664-019-00969-0

 

 

 

Case B:

 

Case of 52 year old man with severe epigastric pain. 

 

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

 

 

Questions:

 

 

1) What is causing the patient's dyspnea? How is it related to pancreatitis?

 

In the pathogenesis of respiratory complications of pancreatitis, inflammatory mediators released from pancreatic injury and digestive actions of pancreatic enzymes play a key role. The role of active digestive enzymes in circulation, release of multiple pro-inflammatory cytokines, activation and migration of leukocytes/neutrophils, complement mediated injury, and platelet activating factors are primarily involved in development of these complication. A damage to the pulmonary vasculature caused by activated trypsin leads to increased endothelial permeability while the main culprit for pulmonary complications.

 

 

2) Name possible reasons why the patient has developed a state of hyperglycemia.

 

β-cell function inversely regulates α-cell function via paracrine mechanisms within the islet, the initial defects in insulin secretion seen in chronic pancreatitis are associated with increases in glucagon secretion that may contribute to early impairment in glucose tolerance, and correlates with an increase in the numbers of islet α-cells observed pathologically. However, with progressive islet damage during the course of T3cDM diabetes, glucagon secretion becomes impaired, which may contribute to the development of brittle diabetes late in the disease.

 

 

3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

 

According to the report the patient has grade I fatty livver due to his chronic consumption of alcohol which might've caused elevated LFT's.

 

The biochemical markers for chronic alcohol consumption that have been most commonly studied are serum GGT, AST, ALT, mean corpuscular volume (MCV) and carbohydrate-deficient transferrin (CDT). An AST to ALT ratio over 2 is highly suggestive of ALD. Most patients with non-ALD have AST to ALT ratios below one. Specific IgA antibodies directed towards acetaldehyde-derived protein modifications are frequently seen alcoholics and thus IgA levels are increased in chronic ALD. An increased ratio of IgA to IgG is highly suggestive of ALD.

 

Chronic alcohol consumption is known to induce a rise in serum GGT and is a widely used index for excessive alcohol use. However, elevated GGT alone has both low sensitivity and specificity for alcohol abuse. GGT is not specific to alcoholism and is increased in many conditions such as obesity, advanced age, moderate alcohol consumption, all forms of liver disease including fatty liver and in particular intra and extrahepatic biliary obstruction, hepatocellular carcinoma and phenytoin use. The sensitivity of GGT as a marker for alcohol consumption in young adults has been showed to be particularly poor even in cases of documented alcohol dependence.

 

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155359/#:~:text=The%20biochemical%20markers%20for%20chronic,ALD%5B85%2C86%5D.

 

 

4) What is the line of treatment in this patient?

 

Treatment:

• IVF: 125 mL/hr 

• Inj PAN 40mg i.v OD 

• Inj ZOFER 4mg i.v sos 

• Inj Tramadol 1 amp in 100 mL NS, i.v sos

• Tab Dolo 650mg sos 

• GRBS charting 6th hourly 

• BP charting 8th hourly 

 

 

 

 

 

 

Case C:

 

A 45 year old Female patient, came to Hospital with cheif complaints of:

·        Fever since 3 days

·        Pain in abdomen since 2 days

·        Decreased urine output since 2 days

·        Abdominal distention since morning

 

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

 

 

Questions:

 

 

1) What is the most probable diagnosis in this patient?

 

The probable diagnosis in this case is Analgesic Nephropathy.

 

 

2) What was the cause of her death?

 

The cause of death in this may be due to sepsis.

 

 

3) Does her NSAID abuse have  something to do with her condition? How?

 

As the patient has Grade III RPD changes in her right kidney she may have an underlying CKD which is secondary to her NSAID abuse.

 

 

 

NEPHROLOGY

 

 

Case A:

A 52 yr old male patient who is a farmer by occupation presented to hospital on 17 May 2021 with  chief complaints of  SOB since 4 days, burning micturition since 4 days and fever since 2 days.

 

https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

 

 

Questions:

 

1. What could be the reason for his SOB ?

 

Chronic kidney disease can lead to anemia which leaves the blood short of red blood cells with which to carry oxygen. Anemia and the need to be more active can lead to our body struggling to get enough oxygen for our muscles and can leave us out of breath.

Kidney disease is one of the more common complications of diabetes, affecting about 40% of people with diabetes.

 

2. Why does he have intermittent episodes of  drowsiness ?

 

A case of slight/mild hyponatremia may cause fatigue, restlessness, confusion and sluggishness. Drowsiness in this patient may be due to hyponatremia because patient showed improvement after administration of sodium.

 

 

3. Why did he complain of fleshy mass like passage in his urine?

 

Fleshy mass like passage in urine is due to pyuria. Pus cells in the urine appear as fleshy mass.

 

 

4. What are the complications of TURP that he may have had?

 

He seems to face electrolyte imbalance post TURP.

 

 

 

Case B:

 

An 8 year old with frequent urination.

 

https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

 

 

Questions:

 

1.Why is the child excessively hyperactive without much of social etiquettes ?

 

The child seems to be psycho somatic, hence the behaviour.

 

 

2. Why doesn't the child have the excessive urge of urination at night time ?

 

The child has excessive urge to urinate during the daytime even though the bladder isn't full because of his psychological impulse to urinate. During the night time he wouldn't have the compulsion to do so since he's asleep.

 

 

3. How would you want to manage the patient to relieve him of his symptoms?

 

I wouldn't recommend any medicines as such because all the reports, clinical findings seem normal. He could be counselled mentally and go to therapy to overcome his psychological compulsion to urinate excessive amount of times even when he doesn't need to. A placebo might be of help.

 

 

 

 

 

 

INFECTIOUS DISEASES

 

 

 

Case A:

 

A 40 year old lady who works in cotton fields came to the hospital with the chief complaints of difficulty in swallowing, fever and cough since 2 months.

 

https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html

 

 

Questions:

 

1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?

 

Characteristic clinical history of tracheoesophageal fistula are :

·        cough

·        difficulty in swallowing

·        loss of weight

·        shortness of breath

Characteristic physical findings of tracheoesophageal fistula are:

·         Fistulous communication between left main bronchus and mid thoracic oesophagus.

 

 

 

 

 

 

 

 

 

 

 

2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

 

 

 

As patient is TB positive, during or after completion of anti-TB therapy, there is a chance of developing tuberculosis immune reconstitution inflammatory syndrome.

 

The most effective prevention of immune reconstitution inflammatory syndrome would involve initiation of ART before the development of advanced immunosuppression.

 

 

https://www.sciencedirect.com/science/article/pii/S2405579415300097

 

 

 

 

 

 

 

 

 

INFECTIOUS DISEASE AND HEPATOLOGY

 

 

Case A:

 

A 55 year old male patient who is a palm tree climber by occupation came on 17th April 2021 with the chief complaints of pain in abdomen since one week, decrease appetite since one week, fever since 2 days.

https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

 

Questions:

 

 

1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?

 

As mentioned patient is chronic alcoholic and smoker. In 50% of the liver abscess cases these are the predisposing factors.

 

 

2. What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)

 

 

 

 

 

3. Is liver abscess more common in right lobe ?

 

50% of solitary liver abscesses occur in the right lobe of the liver (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.

 

 

4.What are the indications for ultrasound guided aspiration of liver abscess ?

 

Indications

·     Complicated diverticular abscess.

·     Crohn's disease related abscess.

·     Complicated appendicitis with appendicular abscess.

·     Tuboovarian abscess.

·     Post-surgical fluid collections.

·     Renal abscess or retroperitoneal abscess.

·     Rplenic abscess.

1) If the abcess is large ( 5cm or more) because it has more chances to rupture.

2) If the abcess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.

3) If the abcess is not responding to the drugs for 7 or more days 

 

 

 

 

Case B:

 

A 21 yr old male student, resident of nakrekal, came to the hospital with chief complaints of abdominal pain since 20 days and fever since 18 days.

 

 

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

 

 

Questions:

 

1) Cause of liver abcess in this patient ?

 

Infection

 

 

2) How do you approach this patient ?

 

 

Antibiotics

 

3) Why do we treat here ; both amoebic and pyogenic liver abcess? 

 

If we dont treate amobic liver abcess there is a chance that one of the following occurs:

 

·        a) Intraperitoneal, intrathoracic, or intrapericardial rupture, with or without secondary bacterial infection.

·     b) Extension to pleura or pericardium.

·     c) Dissemination and formation of brain abscess.

·      

·     If we dont treate pyogenic liver abcess there is a chance that one of the following occurs:

·      

·     a) Sepsis.

·     b) Empyema resulting from contiguous spread or intrapleural rupture of abscess.

·     c) Rupture of abscess with resulting peritonitis.

·     d) Endophthalmitis when an abscess is associated with K pneumoniae bacteremia.

 

 

4) Is there a way to confirm the definitive diagnosis in this patient?

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

HEPATOLOGY

 

CASE A

A 55 year old male patient who is a palm tree climber by Occupation 

came on 17th April 2021 with the chief Complaints of  

PAIN ABDOMEN SINCE ONE WEEK 

DECREASE APPETITE SINCE ONE WEEK

 FEVER SINCE 2 DAYS

 

 

https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

 

 

 

1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?

 

As mentioned patient is chronic alcoholic and smoker. In 50% of the liver abcess cases these ae the predisposing factors.

 

2. What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)

 

 

 

3. Is liver abscess more common in right lobe ?

 

50% of solitary liver abscesses occur in the right lobe of the liver (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.

 

4.What are the indications for ultrasound guided aspiration of liver abscess?

 

Indications

• complicated diverticular abscess.
• Crohn's disease related abscess.
• complicated appendicitis with appendicular abscess.
• tuboovarian abscess.
• post-surgical fluid collections.
• hepatic abscess (e.g. amoebic or post-operative)
• renal abscess or retroperitoneal abscess.
• splenic abscess.

1) If the abcess is large ( 5cm or more) because it has more chances to rupture.

2) If the abcess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.

3) If the abcess is not responding to the drugs for 7 or more days 

 

 

 

 

 

 

 

CASE B

 

CASE DISCUSSION ON LIVER ABCESS

 

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

 

 

1) Cause of liver abcess in this patient ?

 

 

2) How do you approach this patient ?

 

 

3) Why do we treat here ; both amoebic and pyogenic liver abcess? 

•  
• If we dont treate amobic liver abcess there is a chance that one of the following occurs:
• Intraperitoneal, intrathoracic, or intrapericardial rupture, with or without secondary bacterial infection.
• Direct extension to pleura or pericardium.
• Dissemination and formation of brain abscess.
• If we dont treate pyogenic liver abcess there is a chance that one of the following occurs:
• Sepsis.
• Empyema resulting from contiguous spread or intrapleural rupture of abscess.
• Rupture of abscess with resulting peritonitis.
• Endophthalmitis when an abscess is associated with K pneumoniae bacteremia.

 

4) Is there a way to confirm the definitive diagnosis in this patient?

 

 

 

PULMONOLOGY

 

CASE A

 

A 55 year old female patient, a resident of Miryalaguda and farmer by occupation came to the hospital on 17/5/21 with the chief complaints of shortness of breath, pedal edema and facial puffiness.

 

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

 

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

Evolution of symptomatology

 

20 years ago:

Shortness of breath : on of off while working at paddy field

                                       relieved upon taking medication

 

12 years ago:

Episode of SOB : This one lasted 20 days and she had to be hospitalized. The                                          SOB decreased upon treatment at the hospital.(grade II)

 

 

8 years ago

 Similar episodes of SOB every year each lasting approximately 1 week. Relieved upon taking medication

 

Diabetes diagnosed

Polyuria

 

5 years ago:

Anemia treatment with iron injections

 

30 days back

Episode of SOB : insidious in onset and gradual in progression.

                             occurred on exertion and was relieved upon rest. 

Generalised weakness

 

20 days back:

 HRCT outside which showed bronchiectasis

Hyperstension diagnosed

 

15 days back:

Pedal edema : upto the level ankle 

                            pitting type.

Facial puffiness

 

2 days back:

SOB :even at rest (grade IV) 

         not relieved with nebulizers

Drowsiness

 

Anatomical localization 

 

Chronic obstructive pulmonary syndrome

Bronchiectasis

 

 

 

 

primary etiology

 

COPD is caused by prolonged exposure to harmful particles or gases which may include second-hand smoke, environmental and occupational exposures, and alpha-1 antitrypsin deficiency. In this case patiemt is exposed to paddy frequently.

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

3) What could be the causes for her current acute exacerbation?

 

Exacerbations of COPD are thought to be caused by complex interactions between the host, bacteria, viruses, and environmental pollution. These factors increase the inflammatory burden in the lower airways, overwhelming the protective anti‐inflammatory defences leading to tissue damage. 

In this case, patient developed episodes commonly around January, while working in paddy field. dust particles in the paddy field or paddy can be the allergen that is causing the episodes.

 

 

4. Could the ATT have affected her symptoms? If so how?

 

Patient has barrel shaped chest.  Usually barrel shaped chest is seen in emphysema. In emphysema there is ATT deficiency.  So deficiency of ATT could have affected her symptoms.

 

 

 

 

 

 

 

 

5.What could be the causes for her electrolyte imbalance?

 

Serum electrolyte imbalance such as hyponatremia, hypokalemia, hyperbilirubinemia, and elevated levels of transaminases, blood urea, and serum creatinine are either caused by the disease process or the therapy initiated 

 

On Sat, May 29, 2021 at 3:02 PM 183 Sai Shreya Surapaneni <saishreya123@gmail.com> wrote:

NEUROLOGY

 

Case A:  

 

A 40 year old male presented to the hospital from Yadagirigutta with the chief complaints of irrelevant talking and decreased food intake since 9 days. 

 

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

 

Questions:

 

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

EVOLUTION OF SYMPTOMATOLOGY:

 

12 YEARS AGO

·        Addicted to alcohol, drinks about 3-4 quarters per day

2 YEARS AGO

·        Diagnosed with type 2 Diabetes (irregular medication; once in 2 or 3 days)

1 YEAR AGO

·        1-2 episodes of seizures (mostly due to alcohol consumption)

4 MONTHS AGO

·        Developed a seizure (mostly GTCS)

·        Cessation of alcohol for 24 hours assosiated with symptoms of restlessness, sweating, and tremors.

10 DAYS AGO

·        General body pains

9 DAYS AGO

·        Started talking and laughing to himself (sudden onset)

·        Decreased food intake

·        Required assistance to move around

·        Short term memory loss (couldn't recognise family members)

ANATOMICAL LOCALISATION

 

PRIMARY ETIOLOGY

 

·        Wernicke's encephalopathy: thiamine deficiency secondary to alcohol dependence

·        Uremic encephalopathy: 

·        Altered sensorium: alcohol withdrawal syndrome

 

 

 

 

 

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

 

3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

 

 

4) What is the reason for giving thiamine in this patient?

 

 Wernicke’s encephalopathy is an acute neuropsychiatric disorder that occurs as a result of thiamine (vitamin B1) deficiency. Thiamine has been administered to counteract its deficiency.

 

 

5) What is the probable reason for kidney injury in this patient? 

 

Chronic alcohol consumption might have lead to kidney injury in this patient.

 

 

 

6). What is the probable cause for the normocytic anemia?

 

The most common cause of normocytic anemia is a long-term (chronic) disease. In this case, the patient has been suffering from uremic encephalopathy which is an organic brain disorder. It develops in patients with acute or chronic renal failure, usually when the estimated glomerular filtration rate falls and remains below 15 mL/min.

 

7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

 

 

 

 

 

 

Case B:

 

A 52 year old male came to the hospital 2 days back presenting with slurring of speech and deviation of mouth that lasted for 1 day and resolved on the same day. 

 

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

 

Questions:

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

 

3) Did the patients history of denovo HTN contribute to his current condition?

 

 

 

4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?

 

 

 

Case C:

 

A 45 years old female ,house wife by occupation came to opd with chief complaints of palpitations, chest heaviness, pedal edema, chest pain, radiating pain along her left upper limb.

 

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Questions:

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

 

 

 

2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

 

 

 

 

 

 

 

3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?

 

ECG changes include:

·        Flattening and inversion of T waves in mild hypokalemia

·        Q-T interval prolongation

·        Visible U wave and mild ST depression in more severe hypokalemia

·        Severe hypokalemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.

Clinical symptoms of hypokalemia do not become evident until the serum potassium level is less than 3 mmol/L. The severity of symptoms also tends to be proportional to the degree and duration of hypokalemia. 

 

The assosiated symptoms are:

·        Muscle weakness (the pattern is ascending in nature affecting the lower extremities, progressing to involve the trunk and upper extremities and potentially advancing to paralysis).

·        Fatigue

·        Constipation

·        Muscle twitches

·        Palpitations

In more severe cases, abnormal rythms may occurs:

·        Atrial or ventricular fibrillation

·        Premature heartbeats

·        Tachycardia

·        Bradycardia

 

 

 

 

 

Case D:

 

A 55year old male patient came to OPD with c/o altered sensorium and involuntary movements from 11pm and recurrent episodes of seizures since 5yrs.

 

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

 

Questions:

 

1) Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

 

Yes, post‐stroke seizure and post‐stroke epilepsy are common causes of hospital admissions, either as a presenting feature or as a complication after a stroke. Also taking into consideration the age of our patient, it is to be noted that stroke is the most common cause of seizures in the elderly population.

 

Causes for early onset seizures after ischaemic strokes:

·        An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation

·         Glutamate excitotoxicity

·         Hypoxia

·         Metabolic dysfunction

·         Global hypoperfusion

·         Hyperperfusion injury.

Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring. Haemosiderin deposits are thought to cause irritability after a haemorrhagic stroke.

 

 

2) In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

 

The patient might have experienced a grand mal seizure — also known as a generalized tonic-clonic seizure in his last episode.  It is defined as a seizure that has a tonic phase followed by clonic muscle contractions. They are usually associated with impaired awareness or complete loss of consciousness.

 

 

 

 

 

Case E:

 

A 48-year-old gentleman hailing from a small town in Telangana presented to the casualty ward on 25th April 2021 at 7:40am with the chief complaints of unresponsiveness for 7 hours and 3 intermittent episodes of seizures in the past 3 hours.

 

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

 

Questions:

 

1) What could have been the reason for this patient to develop ataxia in the past 1 year?

 

 Ataxia usually results from damage to a part of the brain called the cerebellum, but it can also be caused by damage to other parts of the nervous system. 

 

This damage can be caused by 

·        a head injury

·        lack of oxygen

·         long-term consumption of alcohol.

·        underlying conditions such as MS

 As the patient has a h/o minor head injuries and addiction to alcohol since 3 years, he might've developed ataxia.

 

2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?

 

The probable reasons for IC bleed in this case are:

·        Chronic alcohol abuse assosiated to high blood pressure which can cause the thin-walled arteries which supply blood to the brain to rupture, releasing blood into the brain tissue.

·        Untreated head injuries                                                                                    

Assosiation of alcohol with bleeding disorders:

·        Alcohol has numerous adverse effects on the various types of blood cells and their functions. Heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that cannot mature into functional cells.

·         Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. 

·        Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria.

·         Consequently, alcoholics frequently suffer from bacterial infections. Finally, alcohol adversely affects the platelets and other components of the blood-clotting system. Heavy alcohol consumption thus may increase the drinker's risk of suffering a stroke.

 

 

 

Case F:

 

A 30 year old male patient lorry driver by occupation came to the OPD with chief complaints of weakness of right upper and lower limb since one day and deviation of mouth towards left since one day.

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Questions:

1. Does the patient's  history of road traffic accident have any role in his present condition?

No.

2. What are warning signs of CVA?

·        Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.

·        Sudden confusion, trouble speaking, or difficulty understanding speech.

·        Sudden trouble seeing in one or both eyes.

·        Sudden trouble walking, dizziness, loss of balance, or lack of coordination.

·        Sudden severe headache with no known cause.

3.What is the drug rationale in CVA?

·        Drug treatment of CVA involves intravenous thrombolysis with alteplase. Intravenous alteplase promotes thrombolysis by hydrolyzing plasminogen to form the proteolytic enzyme plasmin. Plasmin targets the blood clot with limited systemic thrombolytic effects.

·         Other acute supportive interventions for CVA include maintaining normoglycemia, euthermia and treating severe hypertension. 

·        Urgent antiplatelet use for AIS has limited benefits and should only promptly be initiated if alteplase was not administered, or after 24 hours if alteplase was administered.

 

4. Does alcohol has any role in his attack?

 

Liver damage in chronic alcoholics can stop the liver from making substances that help blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.

 

5.Does his lipid profile has any role for his attack?

 

No.

 

 

 

 

Case G:

 

50-year-old male patient presented to hospital with complaints of weakness of all four limbs since 8 PM yesterday.

 

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

 

Questions:

 

1) What is myelopathy hand ?

 

A characteristic dysfunction of the hand in cervical spinal disorders with loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers.  It appears to be due to pyramidal tract involvement.

 

 

2) What is finger escape ?

 

It refers to the slightly greater abduction of the fifth digit, due to paralysis of the abducting palmar interosseous muscle and unopposed action of the radial innervated extensor muscles.

 

 

3) What is Hoffman’s reflex?

 

Hoffmann's reflex is a neurological examination finding elicited by a reflex test which can help verify the presence or absence of issues arising from the corticospinal tract. 

 

 

 

 

Case H:

 

A 17 year old female student by occupation presented to causality on 1/5/2021 with chief complaints of involuntary movements of both upper and lower limbs a day before.

 

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1         

 

 

Questions:

 

1) What can be  the cause of her condition ?  

 

 

2) What are the risk factors for cortical vein thrombosis?

·         

·        Risk factors for children and infants include:

·        Beta-thalassemia major

·        Heart disease — either congenital (you're born with it) or acquired (you develop it)

·        Iron deficiency

·        Certain infections

·        Dehydration

·        Head injury

·        Sickle cell anemia

·        For newborns, a mother who had certain infections or a history of infertility

      Risk factors for adults include:

·        Pregnancy and the first few weeks after delivery

·        Problems with blood clotting

·        Collagen vascular diseases

·        Obesity

·        Cancer

·        Inflammatory bowel disease like Crohn's 

·        Low blood pressure in the brain

·      

3)There was seizure free period in between but again sudden episode of GTCS, why? Resolved spontaneously, why?   

 

4) What drug was used in suspicion of cortical venous sinus thrombosis?

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CARDIOLOGY

 

 

 

Case A:

 

A 78 yr old male  patient, resident of  of kattangur and shepherd by occupation came to the OPD  on 14 /5/2021 with chief complaints of:

·        shortness of breath, since 20 days

·        chest pain, since 20 days

·        B/L pedal edema, since 4 days

·        facial puffiness, since 4 days

 

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.

 

 

Questions:

 

 

1.What is the difference between heart failure with preserved ejection fraction and with reduced ejection fraction?

 

 

 

 

 

 

 

2.Why haven't we done pericardiocenetis in this pateint?        

 

Pericardiocentesis is a procedure done to remove fluid that has built up in the sac around the pericardium. In this case, to keep a check if patient is having cardiac tamponade , review of ECHO has been done. As no cardiac tamponade was seen this procedure wasn't performed.

 

 

3.What are the risk factors for development of heart failure in the patient?

 

The risk factors of heart failure are:

·        Hypertension

·        Coronary artery disease

·        Diabetes

·        Certain medication

·        Alcohol abuse

·        Smoking

·        Obesity

·        Congenital heart defects

·        Sleep apnea

 

4.What could be the cause for hypotension in this case?

 

The patient is suffering from acute, rapid accumulation of fluid in the pericardium which causes signs of acute hemodynamic compromise in cardiac tamponade. Patients with this condition develop tachycardia, hypotension and distended neck veins.

 

 

 

 

Case B:

 

A 73 yr male patient teacher by occupation, presented to OPD with  chief complaints of :

·        Pedal edema, since 15 days 

·        Shortness of breath, since 4 days

·        Decreased urine output, since 2 days

 

https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html. 

 

 

Questions:

 

1.What are the possible causes for heart failure in this patient?

 

The probable causes for heart failure in this patient are:

·        Chronic alcohol abuse

·        Long standing case of hypertension (19 years)

·        Stage 4 Chronic Kidney disease

 

2. What is the reason for anaemia in this case?

 

 

 

 

3.What is the reason for blebs and non healing ulcer in the legs of this patient?

 

Leg and foot ulcers in diabetic patients have three common underlying causes: venous insufficiency, peripheral neuropathy, or peripheral arterial occlusive disease.

 

4. What sequence of stages of diabetes has been noted in this patient?

 

 

 

 

               

Case C:

 

A 52yr old male came to the OPD with the chief complaints of decreased urine output and shortness of breath at rest since one day.

 

 

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

 

 

Questions:

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

EVOLUTION OF SYMPTOMATOLOGY

10 YEARS AGO

·        Surgery for inguinal hernia

3 YEARS AGO

·        Aggravated on and off pain at the site of surgery

·        On and off facial puffiness

1 YEAR AGO

·        Grade II shortness of breath - diagnosed for HTN (on medication)

2 DAYS AGO

·        Shortness of breath Grade II (on exertion) 

·        Decreased urine output

·        Constipation

ONE DAY AGO

·        Shortness of breath Grade IV (at rest)

DAY OF ADMISSION

·        Anuria

 

 

ANATOMICAL LOCALISATION

1.      HEART: a) Atrial fibrillation with Rapid ventricular response

                         b) Thrombi noted in Left Atrial Appendages and Left atrium

 

                         c) Dilated Main Pulmonary Artery and Left Pulmonary Arteries

 

                         d) Severe LV dysfunction

                          

                         e) IVC dilated

 

 

      2. KIDNEY: a) Cardiorenal syndrome

 

 

ETIOLOGY OF DISEASE IN PATIENT

·         Loss of Atrial contraction and Left atrial dilatation causes stasis of blood in the LA and may lead to thrombus formation in the Left Atrial Appendage. This predisposes patients to stroke and other forms of systemic embolism - Bilateral thrombosis

·        Cardiorenal syndrome 4 in this patient can be attributed to prior history of heart failure, HTN and age.

·        Abnormal heart rhythms, including atrial fibrillation or atrial flutter, affect 50 to 60 percent of all patients over 40 with an ASD.

 

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

 

1) Drug name:   DOBUTAMINE

 

MOA: Dobutamine directly stimulates beta-1 receptors of the heart to increase myocardial contractility and stroke volume, resulting in increased cardiac output.

 

Indication: Indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures.

 

Efficacy over dobutamine:

·        P- 673 participants

·        I - dobutamine

·        c - out of 673 participants random number of patients are given placebo

·        o - dobutamine is not associated with improved mortality in patients with heart failure, and there is a suggestion of increased mortality associated with its use

       

https://go.drugbank.com/drugs/DB00841

https://link.springer.com/article/10.1007/s00134-011-2435-6

 

 

2) Drug name: CARVEDILOL                                                                                    

 

Mechanism of action: Carvedilol inhibits exercise induce tachycardia through its inhibition of beta adrenoceptors. Carvedilol's action on alpha-1 adrenergic receptors relaxes smooth muscle in vasculature, leading to reduced peripheral vascular resistance and an overall reduction in blood pressure.

 

Indication:  Carvedilol is indicated to treat mild to severe heart failure, left ventricular              dysfunction after myocardial infarction with ventricular ejection fraction or hypertension.

        

Efficacy over Carvedilol :

·        p : 131

·        i : carvedilol

·        c : out of 131 participants random number of patients are given placebo

·        o : The beta-blocker carvedilol can be safely employed in patients with severe heart failure. Improved left ventricular function

https://go.drugbank.com/drugs/DB01136

https://pubmed.ncbi.nlm.nih.gov/9330125/

 

3) Drug name:  UNFRACTIONED HEPARIN

MOA: Administered heparin binds reversibly to ATIII and leads to almost instantaneous inactivation of factors IIa and Xa The heparin-ATIII complex can also inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin is ATIII-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of heparin is well correlated to the inhibition of factor Xa. Heparin is not a thrombolytic or fibrinolytic. It prevents progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.

 

Indication: It is used to prevent embolisms in patients with atrial fibrillation and as an adjunct antithrombin therapy in patients with unstable angina and/or non-Q wave myocardial infarctions 

 

Efficacy over unfractioned heparin:

·        p : 1473

·        i : unfractioned heparin

·        c :  out of 1473 participants random number of patients are given placebo

·        o :  decrase in thromoembolism

https://clinicaltrials.gov/ct2/show/NCT00432796

https://go.drugbank.com/drugs/DB01109

 

4) Drug name: TAB. DYTOR

 

MOA: Torasemide is known to have an effect in the renin-angiotensin-aldosterone system by inhibiting the downstream cascade after the activation of angiotensin II. This inhibition will produce a secondary effect marked by the reduction of the expression of aldosterone synthase, TGF-B1 and thromboxane A2 and a reduction on the aldosterone receptor binding.

 

Indication: Torasemide is indicated for the treatment of edema associated with congestive heart failure, renal or hepatic diseases.

 

Efficacy over dytor:

·        p : 68

·        i : torsemide

·        c : 34

·        o : improvement in peripheral edema

https://pubmed.ncbi.nlm.nih.gov/11862232/

 

5) Drug name: TAB. TAXIM

 

MOA: The bactericidal activity of cefotaxime results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cefotaxime shows high affinity for penicillin-binding proteins in the cell wall including PBP Ib and PBP III.

 

Indication: Used to treat gonorrhoea, meningitis, and severe infections including infections of the kidney (pyelonephritis) and urinary system. Also used before an operation to prevent infection after surgery

 

Efficacy over Taxim:

·        p : 60

·        i : taxim

·        c : out of 60 participants random number of patients are given placebo

·        o :  the results indicate that cefixime twice daily is comparable in safety 

https://go.drugbank.com/drugs/DB00493

https://pubmed.ncbi.nlm.nih.gov/2663735/

 

 

6) Drug name:  INJ THIAMINE

 

MOA: It is thought that the mechanism of action of thiamine on endothelial cells is related to a reduction in intracellular protein glycation by redirecting the glycolytic flux. Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to their each unique biological functions.

 

Indication: For the treatment of thiamine and niacin deficiency states, Korsakov's alcoholic psychosis, Wernicke-Korsakov syndrome, delirium, and peripheral neuritis.

 

Efficacy over thiamine:

·        P : 50

·        I : thiamine

·        C : 25

·        O : Thiamine was not associated to a significant reduction in vasopressor-free days over 7-days in comparison to placebo in patients with septic shock

https://go.drugbank.com/drugs/DB00152

https://bmcanesthesiol.biomedcentral.com/articles/10.1186/s12871-020-01195-4

 

 

 

3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

 

Pathogenesis:

The development of CRS mainly focuses on the inability of the failing heart to generate forward flow, thus resulting in prerenal hypoperfusion. Inadequate renal afferent flow activates the RAAS, the sympathetic nervous system, and arginine vasopressin secretion, leading to fluid retention, increased preload, and worsening pump failure.

The patient is suffering from Type 4 CRS in which CKD leads to heart failure.

 

 

 

 

 

 

 

4) What are the risk factors for atherosclerosis in this patient?

·        Hypertension

·        Bad cholesterol levels

·        Obesity 

·        Diabetes

·        Lack of physical activity

·        Age

·        Smoking

 

5) Why was the patient asked to get those APTT, INR tests for review?

 

The patient was asked to get APTT and INR tests for review as he was prescribed TAB. Acitrom which is a blood thinner and can cause some common side effects such as unusual bleeding from the gums, heavy bleeding from cuts or wounds, unexplained bruising or nosebleeds, heavy periods, abdominal pain, blood vomiting, bloody or black tarry stools.

 

 

 

 

 

Case D:

 

A 67 year old female patient came to the OPD with C/O shortness of breath (SOB) since 1/2 hour.

 

 

https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

 

Questions:

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

EVOLUTION OF SYMPTOMATOLOGY

12 YEARS AGO

·        Diagnosed with type 2 DM (on medication)

1 YEAR AGO

·        Heartburn like episodes (relieved without any medication)

7 MONTHS AGO

·        Diagnosed with TB (completed course of medication)

6 MONTHS AGO

·        Diagnosed with HTN (on medication)

NIGHT BEFORE ADMISSION

·        Sweating on exertion

·        Shortness of breath (at rest)

ON THE DAY OF ADMISSION

·        Shortness of breath since 1/2 an hour

 

ANATOMICAL LOCALISATION

 

 

 

PRIMARY ETIOLOGY:

The increasing population in older age will lead to greater numbers of them presenting with acute coronary syndromes (ACS).he elderly are a high risk group with more significant treatment benefits than younger ACS. Nevertheless, age related inequalities in ACS care are recognised and persist. 

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

1) Drug name: TAB METFORMIN

 

 MOA: Metformin decreases blood glucose levels by decreasing hepatic glucose production, decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization.

 

 Indication: Metformin is indicated as an adjunct to diet and exercise to increase glycemic control in adults and pediatric patients 10 years of age and older diagnosed with type 2 diabetes mellitus.

 

Efficacy over Metformin:

·        p : 451

·        i : metformin

·        c : out of 451 participants random number of patients are given placebo

·        o : Metformin improved glucose variables as compared with placebo. 

https://go.drugbank.com/drugs/DB00331

https://pubmed.ncbi.nlm.nih.gov/9428832/

 

 

 

3) What are the indications and contraindications for PCI?

 

Indications of PCI:

·        Acute ST-elevation myocardial infarction

·        Non–ST-elevation acute coronary syndrome 

·     Unstable angina

·     Stable angina

·     PCI is indicated for the critical coronary artery stenosis, which does not qualify for CABG

Contraindications of PCI:

·        High bleeding risk

·     Intolerance for oral antiplatelets long-term

·     High-grade chronic kidney disease

·     Critical left main stenosis with no collateral flow or patent bypass graft

·     Chronic total occlusion of SVG

 

 

4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?

 

If PCI is performed in a patient who doesn't require it then one of the following may occur:

·        Allergic reaction to the dye/contrast 

·        Kidney damage from the dye/contrast

·        Injury/tears/ruptures of heart arteries

·        Infection, bleeding or bruising at the catheter site

·        Blood clots that can lead to stroke or heart attack

·        Retroperitoneal bleeding

Harms of overtreatment:

·        Psychological stress

·        Financial toxicity

·        Unnecessary care

·        Surgical complications

·        Loss of kidney function

·        Unknown survival benefit

Overtesting, may cause harm to patients and the healthcare system, including through misdiagnosis, false positives, false negatives and overdiagnosis. Clinicians are ultimately responsible for test requests, and are therefore ideally positioned to prevent overtesting and its unintended consequences.

 

 

 

 

Case E:

 

A 60year old Male patient, resident of xxxxxxxx, came to the OPD with the  Chief complaint of chest pain since 3 days and giddiness and profuse sweating since morning. 

 

https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

 

 

Questions:

 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

 

 

EVOLUTION OF SYMPTOMATOLOGY

5 DAYS AGO

·        first dose of  COVISHEILD vaccine

3 DAYS AGO

·        Mild chest pain in the right side of the chest  - pain was insidious in onset                                                                                                                    - gradually progressive                                                                                                                            - pain was of dragging type                                                                                                                      - radiating to the back

·        Dizziness was (not increasing or decreasing with change of position)

·        Profuse sweating

·        Disturbed sleep due to discomfort

                                                                                  

 

 

 

 

 

 

 

ANATOMICAL LOCALISATION

 

ETIOLOGY OF PATIENTS DISEASE

 

 

 

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

 

1) Drug name: ASPIRIN

 

MOA: Blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes . Inhibition of COX-1 results in the inhibition of platelet aggregation

 

 Indication: Due to its ability to inhibit platelet aggregation.

Reducing the risk of cardiovascular death in suspected cases of myocardial infarction (MI)

Efficacy over Aspirin:

·        p: 157 248

·        i : aspirin

·        c : out of 157248 participants random number of patients are given placebo

·        o : Aspirin was associated with a lower incidence of myocardial infarction. associated with an increased incidence of major bleeding

https://academic.oup.com/eurheartj/article/40/7/607/5250614

https://go.drugbank.com/drugs/DB00945

 

2) Drug name: TAB ATROVAS

 

MOA: Atorvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis.

 

INDICATION : Atorvastatin is indicated, in combination with dietary modifications, to prevent cardiovascular events in patients with cardiac risk factors and/or abnormal lipid profiles. Atorvastatin can be used as a preventive agent for myocardial infarction, stroke, revascularization, and angina, in patients without coronary heart disease but with multiple risk factors and in patients with type 2 diabetes without coronary heart disease but multiple risk factors.

 

Efficacy over Atrovas:

·        p : 60

·        i:  atrovastin

·        c : 42

·        o : Atorvastatin lowered LDL-C, apoB, and atherogenic lipoprotein subparticles in children with T1D and elevated LDL-C without worsening insulin resistance. The drug was well tolerated and safe. Long-term studies would provide better insight on the impact of these interventions in the development of cardiovascular disease in children with diabetes.

https://go.drugbank.com/drugs/DB01076

https://pubmed.ncbi.nlm.nih.gov/25418907/

 

3) Drug name: TAB CLOPIB (active metabolite of clopidogrel)

 

MOA: Clopidogrel is metabolized to its active form by carboxylesterase-1. The active form is a platelet inhibitor that irreversibly binds to P2Y12 ADP receptors on platelets. This binding prevents ADP binding to P2Y12 receptors, activation of the glycoprotein GPIIb/IIIa complex, and platelet aggregation.

 

Indication: Clopidogrel is indicated to reduce the risk of myocardial infarction for patients with non-ST elevated acute coronary syndrome (ACS), patients with ST-elevated myocardial infarction, and in recent MI, stroke, or established peripheral arterial disease.

 

Efficacy over Clopib:

·        p : 79,613

·        i : clopidogrel

·        c :  out of 79613 subject placebo is given to random subjects

·        o :clopidogrel was associated with a highly significant 14% proportional reduction in the risk of cardiovascular events

https://go.drugbank.com/drugs/DB00758

https://pubmed.ncbi.nlm.nih.gov/19909874/

 

 

 

3) Did the secondary PTCA do any good to the patient or was it unnecessary?

 

Percutaneous transluminal coronary angioplasty is a surgical treatment to reopen a blocked coronary artery to restore blood flow. It is a type of percutaneous coronary intervention. When performed on patients with acute myocardial infarction, it is called primary angioplasty.

 

After the secondary PTCA the patient was doing better so it was necessary to do.

 

 

 

 

 

 

 

 

Covid-19

CASE-1

Question 1

Interstitial lung diseases (ILDs) comprise a heterogeneous group of acute and chronic lung diseases that cause progressive scarring of the lung tissue, compromising respiratory function and blood oxygenation. The most common form is the idiopathic pulmonary fibrosis (IPF), which in the vast majority of cases affects the older population, in a progressive fibrosing manner, resulting in severe respiratory failure and death within 3–5 years. In patients with preexisting ILD, COVID-19 infection has led to acute exacerbation of underlying ILD. The criteria for ILD exacerbation include subacute worsening of dyspnea and hypoxemia, new pulmonary infiltrates on imaging, and absence of pulmonary emboli, cardiac failure, and other non-pulmonary causes

 

Question 2

Steroid therapy in covid affecting rheumatoid arthritis

There would be no worsening in RA as we already use corticosteroids in treatment of RA

study provides all specialists facing the COVID-19 emergency with a very reassuring message about the possibility of suggesting RMDs patients to continue their current therapy with ts/bDMARDs without an increased risk and probably with a milder infection course. Conversely, the use of GC especially a dose > 2.5 mg per day should be cautiously evaluated during the pandemic.

Steroid therapy in covid affecting hypothyroidism

Steroids are used in treatment of hyperthyroidism which can be condition deepening in hypothyroidism

Question 3

Yes compared to patients with no autoimmune disorders this patient may have

 

Question 4

the role of heparin and low molecular weight (LMW) heparin in this setting has been largely overlooked. the role of heparan sulfate as a key entry mechanism for SARS-CoV-2; the efficacy of heparin and LMW heparin in counteracting its entry into the cell, the recent experimental findings obtained in in vitro studies using the LMW heparin enoxaparin Inhixa®, the role of heparin and LMW heparin in modulating the cytokine storm, and the evidence for the use of LMW heparin in the prevention and treatment of the thromboembolic complications of COVID-19. The available evidence suggests that LMW heparin appears as a promising tool in the treatment of COVID-19. Whether its systematic use is associated with a reduction in complications and ultimately mortality of these patients is being tested in several studies starting worldwide. the virus firstly binds to the abundant HS in the extracellular matrix, increasing its density on the cell surface, and promoting the recognition to its ACE2 receptor. Heparin (100 µg/mL) added 30 min before infection of Vero cells with SARS-CoV reduced the formation of plaques by 50%.the human coronavirus NL63 similar to SARS-CoV-2 S1 RBD undergoes conformational change upon heparin binding, and this decreases the adhesion and hence the interaction with the ACE receptors. Since the interaction with heparan sulfate acts to facilitate ACE receptors binding by virus, it is also possible to block virus cell entry by modulating ACE 2 receptors,

 

 

 

CASE-2

Question 1

protein ACE-2 which binds to SARS-Cov-2 and allows the virus to enter human cells is not only located in the lungs, but also in organs and tissues involved in glucose metabolism such as the pancreas, the small intestine, the fat tissue, the liver and the kidney. by entering these tissues, the virus may cause multiple and complex dysfunctions of glucose metabolism. it is possible that the novel coronavirus may alter glucose metabolism that could complicate the condition of preexisting diabetes or lead to new mechanisms of disease.It is  said virus infections can also precipitate type 1 diabetes - a chronic condition in which the pancreas produces little or no insulin.

 

Question 2

Yes, In covid patients with diabetes there is a risk of release of tissue injury-related enzymes, excessive uncontrolled inflammation responses and hypercoagulable state associated with dysregulation of glucose metabolism which can lead to severe pneumonia these patients also show many pathological changes in hrct scan

Question 3

D dimer - Pulmonary embolism and deep vein thrombosis were ruled out in patients with high probability of thrombosis. D-dimer levels significantly increased with increasing severity of COVID-19 as determined by clinical staging (Kendall’s tau-b = 0.374, P = 0.000) and chest CT staging role of D dimer is to determine the severity and  reliable prognostic marker for in-hospital mortality in patients admitted for COVID-19.

It should be changing management so that anti coagulants or antiplatelet are given to prevent hemorrhagic/ischemic stroke in the patient

 

 

 

 

 

 

 

 

CASE-3

Question 1

Noradrenaline (norepinephrine) is very effective in raising arterial blood pressure and, under almost all circumstances, can be titrated to achieve the desired MAP in a given patient. When given in conscious mammals, renal blood flow is increased and renal vascular resistance decreased in response to infusion.it increase organ perfusion and gfr and renal blood flow  in this way it helpful to manage both hypotension and acute kidney injury at the same time

Question 2

Blood levels of C-reactive protein (CRP) and lactic dehydrogenase (LDH) at the time of non-ICU admission for COVID-19 predict likelihood of adverse outcomes, including development of more serious illness, increased oxygen requirements or ICU transfer. So finds the first detailed characterization of clinical course among COVID-19 patients admitted to a non-ICU setting outside a COVID-19 epicenter, using a remote central monitoring unit (CMU).

“CRP and LDH blood levels can help stratify risk and prioritize resource allocation for non-ICU patients with COVID-19”

Question 3

Advantages of using mechanical ventilation with intubation over other methods include the humidification of oxygen to prevent dehydration of the airway passages, the high flow rates can be used to provide carbon dioxide ‘washout’, there is a reduction in the anatomical dead space and oxygen levels close to 100% can be delivered.

 

CASE-4

Question no 1

ESR – erythrocyte sedimentation rate

As it is related to hemoglobin and c reactive protein and c reactive protein increases in covid infection there was increase in ESR