I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competemcy in reading and comprehensive clinical data including history,clinical findings,investigations and diagnosis and come up with a treatment plan.
This is the link of the questions asked regarding the cases
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Name:J.Sasi Harshith
Roll No:164
Below are the answers to the Medicine assignment based on my comprehension of the cases.
First Case- Pulmonology
Link:
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.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 symptomology:
1 year ago-2 to 3 episodes of seizures
4 months ago-Following cessation of alcohol he developed seizures probably GTCS
9 days back-The patient started talking and laughing to himself
withdrawal seizures are triggered by neuronal networks in the brainstem, including the inferior colliculus
Ethanol is the primary alcohol ingested by chronic users. It is a central nervous system (CNS) depressant that the body becomes reliant on with extended exposure to ethanol. It does this by inhibiting the excitatory portion (glutamate receptors) of the CNS and enhancing the inhibitory portions (GABA receptors) of the CNS. When the depressant is stopped, the central nervous system becomes overexcited as the inhibition is taken away. Thus, the body gets an excitatory overload, which results in the symptoms of withdrawal.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
IVF NS and RL 150ml per hour
aim of lowering alcohol levels and its metabolites, reducing its neuro-depressive effects, and making patents spending less time in the ED.
Thiamine
Thiamine has no effect on the symptoms or signs of alcohol withdrawal or on the incidence of seizures or DTs. Routine use of thiamine is recommended because the development of Wernicke encephalopathy or Wernicke-Korsakoff syndrome is disastrous in these patients and can remain unrecognized. Because orally administered thiamine may have poor enteral absorption in individuals with alcoholism, high-risk patients should receive parenteral thiamine at 100-250 mg once daily for several days.
Lorazepam
are used to treat alcoholism and alcohol withdrawal symptoms
Lorazepam is used by rehab facilities across the nation to help patients overcome an AUD
The drug helps alleviate anxiety associated with alcohol withdrawal. Treatment providers may also prescribe it to reduce the risk of seizures.
Pregabalin
Pregabalin is a high-affinity α2δ voltage-gated calcium channel subunit ligand [23, 24], indicated in different countries for the treatment of neuropathic pain associated with a variety of conditions, fibromyalgia, generalized anxiety disorder (GAD), and as adjunctive therapy for adults with partial-onset seizures
HAI
Human Actrapid 40IU/ml Solution for Injection is a short-acting insulin used to treat type 1 and type 2 diabetes mellitus. It is used together with a healthy diet and regular exercise to control blood sugar levels after meals. This helps to prevent serious complications of diabetes like kidney damage and blindness.
Lactulose
Lactulose is helpful in patients with an acute onset of severe encephalopathy symptoms and in patients with milder, chronic symptoms. This nonabsorbable disaccharide stimulates the passage of ammonia from tissues into the gut lumen and inhibits intestinal ammonia production.
Kcl KCL in NS is a prescription medicine used to treat the symptoms of Hypokalemia, prophylaxisfor Hypokalemia
Potchlor Potklor liquid is used to treat low levels of potassium in the body
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
one of the potential causes could be of right side heart failure.
4) Could the ATT have affected her symptoms? If so how?
No,the att could not have affected her symptoms.
5) What could be the causes for her electrolyte imbalance?
Usually,the patients with heart failure show hyponatremia,hypo magnesiumia, and hypokalemia.
Second case - NEUROLOGY
2Q)patient details link:
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.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?
Type 2 DM - since 2 YRS
Seizures (2-3 eps) - 1month ago
Seizures -4months ago
Short term memory loss -9 days ago
Started talking - 9days ago
Started laughing -9 days ago
He was unable to lift himself off bed - since 9 days
Decreased food intake - since 9days
General body pains -1 day ago
Anatomical localisation :- Brain mainly in the prefrontal cortex,hypothalamus & limbic system.
The primary etiology is the consumption of alcohol.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Electrolyte Replenishmnet is usually done.
Thiamine:It combines with ATP in liver,kidney,leucocytes and produces thiamine diphosphate which helps in transketolation.
Lorazepam:It binds to receptors on GABA in the CNS,this increases the cl channels
Pregabakin:It bind to voltage gated calcium channels and reduce neurotransmitter release.
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
Excessive drinking excites and irritates Nervous System.
Body will be dependent on daily consumption of alcohol.
CNS cannot adapt without alcohol.
Cessation of alcohol leads to alcohol withdrawal symptoms.
4) What is the reason for giving thiamine in this patient?
Alcoholics have thiamine deficiency. As the patient decreased his food intake since 9days ge has been diagnosed as thiamine deficiency as thiamine is not produced in our body.
Thiamine is administered to the patient in order to keep the nervous system healthy
5) What is the probable reason for kidney injury in this patient?
DEHYDRATION is the main cause of the kidney injury.
6). What is the probable cause for the normocytic anemia?
Kidney failure - as erythropoeitin is produced in kidney which plays a key role in the production of RBCs.
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
yes, it has aggrevated the foot ulcer formation due to anaemia caused by alcoholism.
B) Link to patient details:
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?
Giddiness :-7 days back
Giddiness after alcohol consumption :- 3days back
Bilateral Hearing loss :- 3days back
Aural fullness :- 3days back
presence of tinnitus:- 3days back
Vomiting- 2-3 episodes per day
H/o postural instability
Slurring of speech and deviation of mouth :- 1day back (resolved on same day)
Anatomical localisation :-cerebellum
Primary etiology :- alcohol and HTN.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Zofer- prevnets nausea and vomiting
acts by binding to 5-ht3
Atorvastatin-statins reduce cholesterol production
clopidergol-inhibits binding to platelets receptors. this action is irreversible.
3) Did the patients history of denovo HTN contribute to his current condition?
Due to HTN the blood vessels of the patient are damaged.
This can also cause clots,whch can embolize and move to the brain causing a stroke.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Alcohol causes atrial fibrillations leading to stroke.
C) Link to patient details:
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?
Episode of paralysis of both upper and lowerlimbs(rt and left) -10yrs back
right and left paresis due to hypokalemia -1year back
Pedal edema(bilateral)-8 months
blood infection -7 months back
Pain along her left upper limb associated with tingling and numbness-6 days
Palpitations - since 5 days and it is more rapid since yesterday night
Chestpain -since5 days
Difficulty in breathing-5 days
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Reason for recurrence hypokalemia might be due to increased urine output.
Risk factors: - female , low BMI
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms
T-wave :- inversion and flattening (mild)
Q-T interval :- prolonged
Visible U wave
D) Link to patient details:
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?
Seizures after haemorrhagic strokes are thought to be attributable to irritation due to hemosideri deposits caused by products of blood metabolism.
In the case of the late seizures it occurs due to changes in glitoic scaring.
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?
It started with a simple partial seizure which lead to the 'GENERALIZED TONIC CLONIC SEIZURRE'.
E) Link to patient details:
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?
The patient has minor unattended head injuries in the past 1 year. Accoding to the CT scan, the patient has cerebral haemorrhage in the frontal lobe causing, for the occurrence of Frontal lobe ataxia
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
The patient has minor unattended head injuries. During the course of time the minor hemorrhages if present should have been cured on their own. But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal ,Parietal and Temporal lobes.
F) Link to patient details:
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?
Yes,because the Zygomatic arch and the mandibular process are very close to the cranium.
2.What are warning signs of CVA?
Trouble speaking
vison problems
diziness
Co-ordination and balance problems
seizures
severe headaches.
3) What is the drug rationale in CVA?
Mannitol- Because of its osmotic effect, mannitol is assumed to decrease cerebral edema.
Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
Ecosporin can also be used to prevent heart attacks and strokes.
4) Does alcohol has any role in his attack?
In this case alcohol hinder the healing of the minor haemorhages.
5)Does his lipid profile has any role for his attack?
There is a inverse relationship between HDL and stroke.
so the high HDL lower the risk of stroke.
G) Link to patient details:
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
Questions:
1)What is myelopathy hand ?
There is 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. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
2)What is finger escape ?
Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".
3)What is Hoffman’s reflex?
Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.
H) Link to patient details:
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Questions:
1) What can be the cause of her condition?
Cortical vein thrombosis(MRI)
2) What are the risk factors for cortical vein thrombosis?
Infections:
Meningitis, otitis,mastoiditis
Prothrombotic states:
Pregnancy, puerperium,antithrombin deficiency proteinc and protein s deficiency,Hormone replacement therapy.
Mechanical:
Head trauma,lumbar puncture
Inflammatory:
SLE,sarcoidosis,Inflammatory bowel disease.
Malignancy.
Dehydration
Nephrotic syndrome
Drugs:
Oral contraceptives,steroids,Inhibitors of angiogenesis
Chemotherapy:Cyclosporine and l asparginase
Hematological:
Myeloproliferative Malignancies
Primary and secondary polycythemia
Intracranial :
Dural fistula,
venous anomalies
Vasculitis:
Behcets disease wegeners granulomatosis
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
Seizures are resolved and seizure free period got achieved after medical intervention⁷ but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Anticoagulants are used for the prevention of harmful blood clots.
Clexane ( enoxaparin) low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivates factor
CARDIOLOGY
A) Link to patient details:
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.
1)What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency,
whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease
2.Why haven't we done pericardiocenetis in this pateint?
On USG , only a small pocket of 1cm effusion which was obliterating with inspiration was found . As there is risk for lung injury pleural tap has been avoided
3.What are the risk factors for development of heart failure in the patient?
Smoking ,alcohol consumption, high crp levels,dm,htn.
4.What could be the cause for hypotension in this patient?
visceral pericardium may have thickened which is restricting the heart to expand causing hypotension
B) Link to patient details:
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?
Ans)
• Old Age
• Smoking
• High blood pressure
• Alcohol consumption
• Obesity
2.what is the reason for anaemia in this case?
As the pt complaints of decrrased urinary ourput which is due to poor blood flow to the kidneys which results in the less functioning of the kidney.
Erythropoeitin is a hormone produced primarily by the kidney and it plays an important role i RBC production.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Blebs are usually the result of a chronic illness such as heart failure in this patient as he has the cardinak sign i.e. pedal edema
Non healing ulcer is due to venous insufficiency.
4. What sequence of stages of diabetes has been noted in this patient?
STAGE 1: insulin resistance
STAGE 2: prediabetes
STAGE 3:diabetes type 2
STAGE4: microvascular complications
C) Link to patient details:
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?
1st episode of sob -1YR ago (grade 2)
Diagnosed With HTN-1YR ago
2nd episode of sob-2days ago (grade 2to grade 4)
Facial puffiness on and off since 2 to 3yrs
Decreased urine output-since 2 days
Anuria-since morning
ANATOMICAL LOCALIZATION OF PROBLEM-
Left atrium embolisationn
Loss of atrial systolic function (atrial contribution to Ventricular filling is lost)
And Left atrial dilatation causes statis of blood in LEFT ATRIUM and may lead to thrombus formation in left atrial appendage
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
TAB DYTOR 10mg for treating Hypertension
Tab CARDIVAS- Beta blocker
Beta-blockers are used as first line therapy since they reduce the ectopic firing that initiates the arrhythmia. They are particularly useful in patients associated with Coronary artery disease, Hypertension and Cardiac failure.
Rhythm control - IV Flecainide can be used for pharmacological cardioversion and will restore sinus rhythm. (IV Amiodarone if any heart disease present)
TAB DIGOXIN -slows the rate at which electrical currents are conducted from.atria to ventricle
4) What are the risk factors for atherosclerosis in this patient?
Age >45yrs
Hypertension
5) Why was the patient asked to get those APTT, INR tests for review?
APTT -to look out for bleeding disorders like bleeding gums Etc
INR - to see the effects of anticoagulants on clotting system
D) Link to patient details:
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?
• Diabetes melites type 2 - 12yrs
• Heart burn like episode - 1yr
• Pulmonary TB - 7months
• HTN - 6months
• Sweating on exertion& SOB - day before admission
Anatomical localisation :- B.V
Primary etiology :- HTN, AGE
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Tab MET XL 25MG/STAT:- MOA :- long acting BETA-BLOCKER.
It works by relaxing the B.V , showing the heart rate by dping this, it reduces the workload on heart by pumping the blood effectively.
INDICATIONS :- High blood pressurr with angina.
3) What are the indications and contraindications for PCI?
INDICATIONS:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.
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?
People suffer complications including bleeding, blood clots, infection, heart rhythm disturbances and even death from heart attack if PCI is performed in a patient who doesnot need it.
E) Link to patient details:
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:
Uncontrolled DM2 since 8 years
3 days back Mild chest pain dragging type and retrosternal pain(radiated)
Anatomical localisation: Inferior wall of heart
Primary etiology: Diabetes type 2 (uncontrolled)
high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
TAB. ASPIRIN 325 mg PO/STAT
Mechanism of action: The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.
TAB ATORVAS 80mg PO/STAT
Mechanism of action: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
TAB CLOPIBB 300mg PO/STAT
Mechanism of action: The active metabolite of clopidogrelselectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
INJ HAI 6U/IV STAT
VITAL MONITORING.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty
Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times.
F) Link to patient details:
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Patient has been administered I.V fluids which acted as placebo effect
2. What is the rationale of using torsemide in this patient?
Diuretics are used to decrease plasma volume and oedema.
this decreasres cardiac output reuslting in reduction of BP,amd thus reducing peripheral vascular resitance.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Ceftriaxone works by inhibiting the mucopeptide synthesis in the bacterial cell wall.
The beta-lactam moiety of ceftriaxone binds to carboxypeptidases, endopeptidases, and transpeptidases in the bacterial cytoplasmic membrane. These enzymes are involved in cell-wall synthesis and cell division.
It is used as a prophylactic treatment.
4) Gastroenterology (& Pulmonology)
A) Link to patient details:
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?
Pain abdomen and vomiting -5yrs back
Alcohol free period-3yrs
Started alc consumption again-recurrrent episodes of pain abdomen and vomiting(5-6epi)
Increased alcohol consumption (past 20days)toddy
Last Alcohol consumption was 1 week back-he again had pain abdomen and vomiting from 1week
Fever-from 4 days
(High grade)
Constipation, burning micturation -since 4days
Anatomical localization :pancreas
Cause of pancreatitis-may be due to alcohol
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?
INj MEROPENAM -Broad spectrum antibiotic
Inj.METROGYL -Nitroimidazole drug
Inj.AMIKACIN -Aminoglycoside antibiotic
All the above mentioned 3 antibiotics are used to control infection and to prevent septic complications of acute pancreatitis
Total pancreatic nutrition(TPN)--fluids are given to vein,it provides most of the nutrients body needs
TPN has proteins,carbohydrates, fats,minerals,vitamins
IV NS/RL at the rate 12ml/hr-treat dehydration
Inj OCTREOTIDE -Used here to decrease exocrine secretion of pancreas and it also has anti inflammatory effects
INJ.PANTOP -PPI used for its anti pancreatic secretory effect
INJ.THIAMINE -B1 supplement
It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency
ING. TRAMADOL
It is an opioid analgesic, given to releive pain.
B) Link to patient details:
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?
Acute pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia, acute respiratory distress syndrome, atelectasis, and pleural effusion. The pathogenesis of some of the above complications is attributed to the production of noxious cytokines
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Hyperglycemia develops rather often in the early phase of acute pancreatitis, mainly in patients with severe disease [1–3]. This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress or the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells [4–7].
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Elevated liver enzymes in the setting of acute pancreatitis point toward choledocholithiasis as the cause, with an alanine aminotransferase greater than three times the upper limit of normal having a positive predictive value of 95% for gallstone pancreatitis
In heavy drinkers, serum GGT, AST, ALT, ferritin and albumin were all significantly higher than in moderate drinkers or abstainers
4) What is the line of treatment in this patient?
Clinicians employ goal-directed fluid therapy with either normal saline or lactated Ringers, give timely analgesics and antiemetics, and replete electrolytes as needed. The current recommendations are also to initiate feeding trials within 24 hours of disease onset instead of keeping the patient nill per mouth (NPO). There are no clear indications for the type of diet, but typically small low-fat, soft or solid meals correlate with shorter hospital stays than starting a clear liquid diet with slow advancement to solid meals. Enteral feeds via a feeding tube are preferred to total parenteral nutrition in patients unable to tolerate PO.
C) Link to patient details:
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Questions:
1) what is the most probable diagnosis in this patient?
Ruptured liver abscess
2) What was the cause of her death?
Spontaneous gas-forming pyogenic liver abscess (GFPLA) is a rare complication with a high fatality rate in spite of aggressive management. Clinical spectrum of GFPLA can mimic hollow viscus perforation as it usually accompanied by pneumoperitoneum and peritonitis.
3) Does her NSAID abuse have something to do with her condition? How?
NSAIDs rarely affect the liver
NSAIDs are absorbed completely and undergo negligible liver metabolism.
5) Nephrology (and Urology)
A) Link to patient details:
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
1. What could be the reason for his SOB ?
Since the patients creatinine levels are very high, functioning of the kidney is reduced. This causes for the accumulation of fluid in the lungs and thus causes SOB.
2. Why does he have intermittent episodes of drowsiness ?
In healthy individuals, sleep is accompanied by a decrease in sympathetic activity and an increase in vagal tone that leads to a nocturnal dipping of blood pressure
In any kind of kidney related problem it exhibit sympatho-vagal imbalance due to baroreceptor reflex function impairment in which there is hyperactivity of the sympathetic nervous system and decreased vagal tone.
3. Why did he complaint of fleshy mass like passage in his urine?
Creatinine is a normal waste product that the body produces every day during muscle movements and when digesting meat.
When creatinine is very high it probabaly means that high waste product of muscle is being formed and this might result in fleshy mass like passage.
4. What are the complications of TURP that he may have had?
Transylurethral resection of prostate (TURP)
Bladder injury
Bleeding
Blood in the urine after surgery
Electrolyte abnormalities
Infection
Loss of erections
Painful or difficult urination
Retrograde ejaculation (when ejaculate goes into the bladder and not out the penis)
B) Link to patient details:
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 ?
Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age
For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).
2. Why doesn't the child have the excessive urge of urination at night time ?
Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder
3. How would you want to manage the patient to relieve him of his symptoms?
Bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder
To treat attention deficit hyperactivity disorder:
For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents. Schools can be part of the treatment as well.
Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.
Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.
● Question no. 6 : Infectious diseases
Link -
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?
clinical history and physical findings in this patient are positive for -
▪︎Cough since 2 months on taking food and liquids and regurgitation of food seen.
▪︎Difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
▪︎H/O weight loss of 10 Kgs since 2 months, hoarseness of voice, inadequate sleep since 2 months
▪︎Laryngeal crepitus positive
All the above findings are very much indicative of tracheo esophageal fistula.
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
IRIS:this is usually seen in AIDS after iniiating ART therapy in the hiv infected or immuno compromised patients.
risk factors:
>low cd4 count
>disemmated OI
>paucity of inflammatory response
>short duration of sub optimal tretament
In this patients case ART was done 2 months back,complaints were recieved.
this leads to clinical deteriotion amd IRIS.
7) Infectious disease and Hepatology:
Link to patient details:
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 ?
yes, it could be due to intake of contaminated toddy
2)what is the etiopathogenesis of liver abscess in a chronic alcoholic patient?(since 30 yrs - 1 bottle/day)
According to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
3)is liver abscess is more common in right lobe?
yes right lobe is involved due to its moreblood supply
4) what r the indications for usg guided aspiration of liver abscess
Indications for USG guided aspiration of liver abscess
1. Large abscess more than 6cms
2. Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugssuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
B) Link :
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS:
1) Cause of liver abcess in this patient ?
■ Single abcess,
■ Right lobe involvement,
■ Route of ingestion is orofecal route
2) How do you approach this patient ?
▪︎ INJECTION. ZOSTUM 1.5 gm IV BD (twice daily)
Zostum is a combination of drugs - SULBACTUM (pencillin) & CEFOPERAZONE(cephalosporin) [Antibiotic]: It is used here to treat if any bacterial cause
▪︎ INJECTION. METROGYL 500mg IV TID ( thrice daily )
Metrogyl has the drug called METRONIDAZOLE [Antibiotic]: For amoebic cause
▪︎ INJECTION. OPTINEURIN 1amp in 100 ml NS( Nor
mal Saline) IV OD ( once daily)
Optineurin is a multivitamin drug { A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement
▪︎ TAB. ULTRACET 1/2 QID( four times a day)
Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and fever
▪︎ TAB. DOLO 650 mg SOS (if needed) given for fever and pain
▪︎ We donot aspirate the pus since it is self resolving and aspiration is associated with several other complications.
3) Why do we treat here ; both amoebic and pyogenic liver abcess?
▪︎We treat both amoebic and pyogenic liver abscess emperically as there is no distinguished clinical features
▪︎ we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.
▪︎ we administer patient with analgesic and antipyretic such as tab.dolo &tab.Ultracet.
4) Is there a way to confirmthe definitive diagnosis in this patient?
■ (Anti amoebic antibodies )ELISA is the confirmatory investigation.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
A) Link to patient details:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.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?
Symptoms-
▪︎Fever since 10 days
▪︎facial puffiness and periorbital edema after 6 days associated with weakness in right upper and lower limb
▪︎ following which he developed altered sensorium 2days later
■ Anatomical position -
Orbit and maxillary sinus
■ Primary etiology-
Infection in a immunocompromised patient .
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?
▪︎ I would like to start the patient on Amphotericin b
As of now , there is no proper study made showing proper efficacy of drugs like Amphotericin b but till date this has shown promising results.
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
▪︎ Due to the rise of covid 19 infections in the country , an excessive surge in patients with comorbities like HTN and most importantly diabetes a very important predisposing factor for the development of mucormycosis.
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