Online blended bimonthly assignment toward summative assessment for the month of May 2021
I have been given the following cases to solve in an attmept to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and coem 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
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
1) pulmonology
A. Link given :
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 symptamology:
1st episode of sob - 20 yrs back
2nd episode of sob - 12 yrs back
She is having yearly episodes of sob from 12 yrs
Diabetes- 8 yrs ago
Anemia and took iron injections - 5ys ago
Generalised weakness - 1month back
hypertension -20 days back
Pedal edema - 15 days back
facial puffiness - 15 days back
# ANATOMICAL LOCALIZATION -lungs
# primary etiology - chronic usage of chulha since 20 yrs
2.What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
*HEAD END ELEVATION -
#MOA : improves oxygenation
Decreases incidence of vap
Decreases incidence of aspiration
Increases end expiratory lung volume performance
Increases hemodynamic performance
# INDICATION:
Pneumonia
Meningitis
Head injury
* OXYGEN INHALATION TO MAINTAIN SPO2
*BIPAP- non invasive method
It assists ventilation by positive expiratory and inspiratory pressure without need of endo tracheal intubation.
3.What could be the causes for her current acute exacerbation?
*it may be due to any infection
4.Could the ATT have affected her symptoms? If so how?
*yes, rifampicin and isoniazid are the nephrotoxic drugs
Raised RFT is seen.
5.What could be the causes for her electrolyte imbalance?
* renal function disturbances due to use of ATT therapy .
2) Neurology
A) links given:
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?
* seizures - 1yr ago and recently 4 mon back
* irrelevant talking - since 9 days
* decreased food intake- since 9 days
* short term memory loss - since 9 days
# ANATOMICAL LOCALIZATION-
Lesion in the brain
# primary etiology - alcohol intake
2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
*THIAMINE- it is a cofactor enzyme in carbohydrate metabolism
Is is used in thiamine deficiency
*LORAZEPAM- it is benzodiazepine receptor antagonist , it enhance the inhibitory GABA effect which increases the chloride ion conductance
It is used generally for seizures
*PREGABALIN- it reduces the synaptic release of neurotransmitters ,and to reduce neuronal excitability & seizures
*LACTULOSE- it acts by decreasing the intestinal production and absorption ammonia.
It is used to treat clinical portal systemic encephalopathy
*PORTCHLOR- liquid 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?
*Due to excess thiamine deficiency and excess toxins accumulation due to chronic alcoholic addiction
4) What is the reason for giving thiamine in this patient?
*Chronic Alcoholism causes thiamine deficiency by impairing the absorption through intestine .
Thiamine acts as cofactor enzyme for carbohydrate metabolism.
Deficiency causes accumulation of products like lactate and pyruvate
This causes wernicke's encephalopathy.
Thiamine is given to treat the deficiency of it.
5) What is the probable reason for kidney injury in this patient?
*Renal system function is to filter the harmful substances.Alcohol disturbance in function of kidney and make less able to filter the blood
It also causes hormones disruption and affect the kidney.
6). What is the probable cause for the normocytic anemia?
*Alcohol causes iron deficiency it affects the production on new blood cells organs i.e ; bonemarrow and show affect on metabolism of iron
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
*Yes,Moreover he is diabetic and and alcohol also weakens the immune system and affect the blood cell production and iron absorption ,dampens yhe healing process.
B) link given:
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
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 symptamology -
- h/o giddiness ( 7 days back) and subsided briefly, and associated with vomiting (1episode).
Then he consumed small amount of alcohol after 3 days and developed giddiness again.
- this associated with bilateral hearing loss, aural fullness,tinnitus
And also vomitings ( 2 - 3 episodes/ day )
H/O postural instability
- slurring of speech and deviation of mouth ( 2 days back )
#ANATOMICAL LOCALIZATION - infarct in the inferior cerebellar hemisphere of the brain.
# primary etiology- hypertension (not on medication) lead to stroke and infarct in the cerebellum due to deprivation of o2.
-Also alcohol abuse.
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 VERTIN - it is an anti vertigo medication.
#Acts as H1receptor agonist present on bv of inner ear ,relaxes the blood vessels and increase the permeability.
#used in balancing disorders.
*TAB ZOFER- it is an anti emetic drug.
# Acts as 5H3 receptor antagonist on vagal afferents of gut and also on the CTZ and solitary nucleus.
#used in vomitings and nausea.
3) Did the patients history of denovo HTN contribute to his current condition?
*Hypertension( left untreated ) can be major risk factor for causing cerebellar infarct, due to increase in sheer stress ,the adaptive responses impair and cause endothelial dysfunction leads to formation of blood clots leads to infarcts.
Yes the history of denovo hypertension contribute to his current condition.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
*chronic alcoholism may impair fibrinolysis and promote the formation of clot by platelet formation.
C) link given:
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.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?
*bilateral pedal edema
* pain along her left upper limb associated with tingling and numbness
*chest pain
*difficulty in breathing
#ANATOMICAL LOCALIZATION - heart
# primary etiology - hypokalemia
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
*pedal edema is the reason for recurrence of hypokalemia
Risk factors- age, female gender
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
*flattening and inversion of T wave
* ST segment depression
* QT interval prolongation
D) link given :
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
*Yes,seizures after ischemic stroke-increase in intracellular Na+ and ca+2 causing depolarization ,glutamate exictability,hypoxia,hyperperfusion injury
- seizures after hemorrhagic ,blood products may cause irritation .
Late onset of seizures cause gliotic scarring,due to persistent neuronal excitability.
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?
*previously,simple partial seizures( no loass of consciousness) have occured
Recently ,GTCS( LOSS of consciousnes) have occured.
E) link given:
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
* Multiple falls may be the reason for to develop ataxia .It is because of head injury which affecting cerebellar dysfunctions causing ataxia.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
* IC bleed is due to head injury
* Yes, alcohol leads to the liver damage where the coagulation factors are produced → this decreases the concentration of clotting factors lead to bleeding diathesis.
F) link given:
http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html
1.Does the patient's history of road traffic accident have any role in his present condition?
* The closeness of facial bones and cranium would suggest that there are chances of cranial injuries
* Zygomatic arch and mandibular process closeness to the cranium would be the reason for patients condition.
2.What are warning signs of CVA?
*Difficulty in walking
* dizziness
* loss of balance and coordination
* blurred visions and difficulty in speaking
3.What is the drug rationale in CVA?
*INJ Mannitol 100 ml iv
*Tab. ecospirin
*Tab atorvas
4. Does alcohol has any role in his attack?
*When patient met with the accident ,there may be cranial damage which is unnoticed
Alcohol hinder the process of hemorrhage and healing.
Patient is not chronic alcoholic so there may be no role of alcohol in his attack.
5.Does his lipid profile has any role for his attack??
*There is an inverse relation b/w HDL -c and ischemic stroke .
The high levels of hdl -cmay lower the risk of stroke.
G) link given:
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
1)What is myelopathy hand ?
* Loss of power of adduction and extension of ulnar two or three fingers and an inability to grip and release rapidly with these fingers , appear to be due to pyramidal tract involvement .
2)What is finger escape ?
*Involuntary abduction of 5th finger caused by unopposed action of extensor digiti minimi @ Wartenbergs sign .
3)What is Hoffman’s reflex?
Neurological examination done to examine the reflexes of upper extremities
H) link given:
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
1) What can be the cause of her condition ?
* Cortical vein thrombosis with hemorrhagic venous infarction and iron deficiency anemia. 2) What are the risk factors for cortical vein thrombosis?
* Sickle cell anemia
*Hemolytic anemia and thalasemia
* CHD , infections , dehydration, iron deficiency
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why? *seizure free period and resolved spontaneously because of medical intervention and sudden episode may be due to persistent excitability and abnormal firing of neurons.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
* INJ clexane 0.4 ml sc
3) cardiology
A) link given:/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?
Ans: preserved ejection fraction - diastolic heart failure(Muscle contracts but ventricles donot relax)
Reduced ejection fraction - systolic heart failure(Muscle doesnot contract effectively).
2.Why haven't we done pericardiocenetis in this pateint?
Ans: The patient diagnosed as heart failure which is post MI with moderate pericardial effusion
POST MI IS CONTRAINDICATION OF PERICARDIOCENTESIS due to risk of scarring and injury.
3.What are the risk factors for development of heart failure in the patient?
Chronic alcoholic , smoker ,with hypertension comorbidity.
4.What could be the cause for hypotension in this patient?
Hypotension may be due to
DIASTOLIC DYSFUNCTION and LV COLLAPSE.
B) link given:
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html
1.What are the possible causes for heart failure in this patient?
Ans: causes-
* patient has stage 4 CKD- has pedal edema ( increased preload)
* Hypertension since 19 yrs
2.what is the reason for anaemia in this case?
Cause-
* chronic kidney disease leads to kidney damage →decrease erythropoietin production from kidney →erythropoietin is low→RBC count drops →ANEMIA develops.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Type 2 diabetes is reason for non healing ulcer and bleb formation
4. What sequence of stages of diabetes has been noted in this patient?
For 26 yrs: diabetes (controlled by tablets)
↓
Since 4yrs: on insulin
↓
Stage 4 DBCD with vascular malformations with retinopathy
C) link given:
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.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?
Facial puffiness ( since 2 to 3 yrs)
Sob grade 2( 1yr ago)
Sob grade 2( 2days back again)
Sob grade 4
Decreased urine output ( since 2 days)
Anuria (since morning)
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
DOBUTAMINE-
*MOA: acts on beta 1 receptor
Beta1 ionotropic effect → increases heart contractility → increases cardiac output
*INDICATIONS: cardiogenic shock , Reversible heart failure
DIGOXIN-
*MOA: 
* INDICATIONS- Atrial fibrillation ,atrial flutter,
Heart failure,Abortion
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 of cardiorenal syndrome
4) What are the risk factors for atherosclerosis in this patient?
Hypertension
5) Why was the patient asked to get those APTT, INR tests for review?
Because of Thrombosis.
To check on development of thrombosis.
D) link given:
https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1
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?
*Heart burn like episodes ( since 1 yr)
* Tb ( 7 months ago)
* SOB ( half n hr before coming to hospital)
##ANATOMICAL LOCALIZATION- coronary artery
## primary etiology- plaque formation or clot formation , 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?
* MOA: relaxes Bv → decreases load on heart → decreases BP
* INDICATIONS- angina ( chest pain )
Heartfailure
Cardiac arrythmias
3) What are the indications and contraindications for PCI?
*percutaneous coronary intervention( PCI)
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?
*PCI cause several complications like :
-Severe bleeding
-blood vessel damage
- allergic reactions to the used contrast dye
-arrythmias
TO Avoid these complications we dont do the pci in the patient who doesnot need it.
* Research on overtesting and over treatment is important to current health system:
It increase the economic burden on the health care system due to excess use of machinaries for investigations .
E) link given:
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
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?
*chest pain - since 3 days
* giddiness and profuse sweating - morning after admission
# ANATOMICAL LOCALIZATION- inferior wall of heart ( ventricle)
# primary etiology - atherosclerosis
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
*MOA: it is a COX inhibitor → which inhibits prostaglandin formation → prevents inflammation ,swelling, pain
* INDICATIONS-
• Fever
• Relieve mild to moderate pain such as tooth ache ,muscle ache ,common cold
ATORVAS-
*MOA: It is a HMG Co A reductase inhibitor
It inhibits conversion of HMG Co A ⟶ mevalonic acid .
* INDICATIONS-
• High cholestrol
• lower the risk of heart attack , stroke, any heart complications
• coronary heart disease
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Yes ,it does good to the patient
F) link given:
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?
Because of the fluid lossoccured to the patient
There is
Decreased preload → SOB occured due to decreased cardiac output
IV fluids administered → there is increase in preload → SOB decreased due to better cardiac output
2. What is the rationale of using torsemide in this patient?
Torsemide is used due to abdominal distension
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Treatment for UTI
Rationale - used for any bacterial infection .
A) link given:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.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 symptamology-
*pain abdomen and vomitings (5 yrs back) with chronic alcohol history.
*Then he stopped taking alcohol and he is symptom free for 3 yrs.
*Then he again developed pain abdomen and vomitings ( 5-6 episodes for past 1 yr) after continuation of alcohol.
* He has increased amount of consumption of alcohol for the past 20 days,Last binge of alcohol is 1 week back.
*Then he again developed pain abdomen and vomiting - since 1 week.
*Fever- since 4 days
*Constipation -since 4 days
*Burning micturition -since 4 days
#ANATOMICAL LOCALIZATION -pancreas.
#primary etiology-alcohol consumption
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?
*Non pharmacological interventions - to drain (malecot & icd)
Even i will follow the same approach as a treating physician.
B) link given:
https://nehaelogs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
*pleural effusion is cause for patients dyspnea.
*pleural effusion may occur due to pancreaticopleural fistulae secondary to leak and disruption of pancreatic duct .
2) Name possible reasons why the patient has developed a state of hyperglycemia.
* Hyperglycemia is developed due to abnormalities in insulin secretion , increase in counter regulatory hormone release ,decreased utilization of glucose by peripheral tissue.
Exocrine pancreatic dysfunction impairs the endocrine pancreas.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
*If serum liver enzymes are elevated ,the gallstone gets lodged down in the distal end of pancreatic duct called choledocholithiosis is the causative factor.
*specific marker for alcoholic fatty liver disease-
GGT,AST,ALT,carbohydrate deficient transferrin, * AST to ALT ratio is highly suggestive for alcoholic liver disease.
4) What is the line of treatment in this patient?
* iv fluids and colloids to maintain normal intravascular volume.
*Nil orally
*Analgesics for pain relief
*Nasogastric suction -to decrease gastrin release from stomach
* Monitor
-BP, pulse,blood sugars ,serum amylase, serum lipase ,urine output.
* laparotomy and debridement of hemorrhagic pancreatic tissue.
* antibiotic therapy like ciprofloxacin , ofloxacin, imipenem
C) link given:
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
1) what is the most probable diagnosis in this patient?
*differential diagnosis -
-Ruptured liver abscess
-intra peritoneal hematoma
-grade 3 RPD of right kidney
-organized collection secondary to hollow viscous perforation
The most probable diagnosis is abdominal hemorrhage causing abdominal distension
2) What was the cause of her death?
* due to emergency laparotomy - complications like infection , hemorrhage ,multiple organ failure may have occured
3) Does her NSAID abuse have something to do with her condition? How?
*acute NSIADS use - may cause induced renal dysfunction leads to decresed renal perfusion , decresed GFR ,acute renal failure
chronic NSAIDS use - may cause hepatotoxicity.
It also causes gastro intestinal injury also.
5) Nephrology
A) link given:
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
1. What could be the reason for his SOB ?
* His is due to acidosis which was caused by using diuretics.
2. Why does he have intermittent episodes of drowsiness ?
*Hyponatremia was the cause for intermittent episodes of drowsiness.
3. Why did he complaint of fleshy mass like passage in his urine?
*Plenty of pus cells in his urine passage appeared as fleshy mass like passage.
4. What are the complications of TURP that he may have had?
*Difficulty in micturition
*infection
*Electrolyte imbalances
B) link given:
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
1.Why is the child excessively hyperactive without much of social etiquettes ?
*Attention deficit hyperactivity disorder(ADHD)- is a neurodevelopmental disorder characterized by inattention ,excessive activity or impulsivity may be the reason for to be child excessively hyperactivity.
2. Why doesn't the child have the excessive urge of urination at night time ?
*child doesn't have the excessive urge of urination at the night but at day time might be due to some psychiatric problem -
-pyschosomatic disorder
-Undiagnosed anxiety disorder
3. How would you want to manage the patient to relieve him of his symptoms?
*For overactive bladder - anti cholinergic drugs
*For ADHD- behaviour therapy and medication for children 6yrs and older.
- methyl phenidate
-amphetamine
6) Infectious diseases ( hiv,mycobacteria,gastroenterology,pulmonology)
A) link given:
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
*Clinical history:
Cough on taking foods and liquids which was initially non productive then associated with sputum which is white in colour and non foul smelling.
Difficult in swallowing since 2 months with solids and liquids. Patient is on RT feeding.
History of weight loss and SOB
One episode of vomiting
Fever episodes
Physical finding:
Thinly built and malnourished
Respiratory system examination: Wheeze present in bilateral mammary areas.
Neck examination: laryngeal crepitus- positive
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
* chances of IRIS are less
IRIS:
The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.
Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS.
7) infectious disease and hepatology
A) link given :
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 ?
*Yes, it could be due to drinking contaminated toddy.
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
*etiopathogenesis-
It is may be due to drinking locally prepared alcohol- which is a predisposing factor for both amoebic liver abscess and pyogenic liver abscess.it is due to the effect of alcohol on liver.
3. Is liver abscess more common in right lobe ?
*yes,Right lobe is more involved due to ots more blood supply
4.What are the indications for ultrasound guided aspiration of liver abscess ?
*Indications-
-large liver abscess more than 6 cm
- left lobe abscess
-caudate lobe abscess
-Abscess which is not responding to drugs
B) link given:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
1) Cause of liver abcess in this patient ?
* cause of liver abscess -
• The most possible cause is because of consuming locally brewed alcohol .
Alcohol has role in facilitating extra-intestinal invasion of protozoanand subsequent development amoebic liver abscess.
2) How do you approach this patient ?
*The patient is well treated by the team ,even we will follow the same approach
3) How do you treat her, amoebic and pyogenic liver abcess?
*Considering some factors -
age and gender( 21 yrs and male)
Single abscess
right lobe involvement
#Most likely it is amoebic liver abscess
But on examination it has no bowel sounds and stool examination for ova and parasite antigen test is insensitive .
# Risk factors on aspiration of pus -
-It may be not accessible to aspirate ,when its is present in the posterior aspect
-due to thin wall , ruptures on aspiration
-it may be unliquefied
# Due to this factors ,we cannot confirm the amoebic / pyogenic liver abscess,treated empiricaly in clinical practice.
4) Is there a way to confirm the definitive diagnosis in this patient?
*yes, we can confirm the diagnosis in high resources using multiple diagnostic strategies, blood culture,entamoeba serology.
8) infectious diseases ( otorhinology,mucormycosis)
A) link given:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.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?
*3 years ago - diagnosed with hypertension
* 21 days ago recieved vaccination and presented with fever , chills and rigors
* 18 days ago again with similar complaints
*11 days ago - c/o generalised weakness ,facial puffiness and periorbital edema.The patient in drowsy state.
*4 days ago- altered state with facial puffiness and periorbital edema,
€ Progressed periorbital edema
€ serous discharge from left eye- blood tinged
€ diagnosed - diabtes mellitus.
* patient died 2 days ago
#ANATOMICAL LOCALIZATION-eye( Mucormycosis) and infarct in the left temporal lobe.
https://www.cdc.gov/fungal/diseases/mucormycosis/definition.html
#Primary etiology- diabetes
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?
*The proposed management of the patient:
a) inj. liposomal amphotericin
b) 200mg itraconazole which was adjusted to his creatinine clearance
C) deoxycholate
*https://pubmed.ncbi.nlm.nih.gov/23729001/
The article tells us about the efficacy and different formulations of liposomal amphotericin.
#Other symptoms management -
Management of Diabetic keto acidosis:
- fluid replacement
- insulin therapy
-electrolyte replacement.
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
*Mucormycosis may be triggered by the use of steroids in the covid 19 patients.
Steroids reduce the inflammation in the covid infected lungs.
This also rises the blood sugar levels in the steroid using patients and lowers the immunity .
With covid 19 rising cases there is increase in occurrence of mucormycosis.
9) infectious diseases( covid19)
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
1) Sort out these detailed patient case report logs into a single web page as a master chart
2) In the master chart classify the patient case report logs into mild, moderate severe and
3) indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension etc).
10) Medical education
Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging of one's own experiences is a vital tool toward competency development in medical education and research. A sample answer to this last assignment around sharing your experience log of the month can be seen in the link below but while this is by a student onsite in hospital and not locked down at home we would be very interested to learn about your telemedical learning experiences from our hospital as well as community patients over the last month even while locked down at home: https://onedrive.live.
Comments
Post a Comment