Medicine blended assignment.
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 come up with a treatment plan.
Pulmonology
A) Link to patient details:
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?
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?
4. Could the ATT have affected her symptoms? If so how?
5.What could be the causes for her electrolyte imbalance?
1.》20 years ago – 1st episode of shortness of breath.
》Similar episodes for next eight years.
》12 years ago – more excacerbation of shortness of breath – hospitalized
》Similar episodes for the next 12 years
》 diagnosed with diabetes 8 years ago
》diagnosed with anemia 5 years ago
》generalized weakness satarted a month ago
》diagnosed with hypertension 20 days ago
》pedal edema 2 weeks ago
》Puffiness of face 2 weeks ago
Anatomical location of problem
》 Lungs (lower segments to be precise)
Primary etiology
》It is by continuos exposure of allergen .
which could be excacerbated by weather.
2.
》Head end elevation-
Improves oxygenation
Deccreases incidence of aspiration.
Indication- Head injury, meningitis, pneumonia.
》O2 therapy to maintain SPO2 above 92%-
》Intermittent BiPAP for 2hrs
Assist ventilation without needing intubation.
》AUGMENTININ : antibiotic pencicillin combined with clavulanic acid. Penicillin acts efficiently against gram positive by inhibiting protien synthesis and blocking ribosomalpathway clavulanic acid enhances the action of penicillin by inhibiting penicillinase enzyme which can produced by resistant bacteria over a period of time
》AZITHROMYCIN : given to treat suspected bacterial infection
》LASIX : its a diuretic to reduce pedal edema and facial puffiness.
》HYDROCORTISONE : steroid to reduce inflammatory andlimiting fibrosis and also decraesing further progression of the disease.
》BUDECORT. is to provide immediate reilief during acute attacks of dyspnea.
It is steroid and has anto inflammatory effect
》GRBS to monitor the blood sugar levels of the patient he was diagnosed with diabetes.
》THIAMINE: given prophylactic to prevent its deficiency.
3.Secondary bacterial infection on exposure of pollen allergen.
4.No
5.Drug induced hyponatremia as the patient is treated for HT by telmisartan.
Neurology A
Link to patient details:
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?
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?
5) What is the probable reason for kidney injury in this patient?
6). What is the probable cause for the normocytic anemia?
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Couple of episode of seizures, in last 1 year and the latest was 4 months back whicb occured following cessation of alcohl intake for 24 hours,
It was associated with restlessness, sweating, and tremors. Aymptoms resolved after he started drinking
Generalised weakness which the patient was unable to support himself associated with decrease food intake for 9 days
had short term memory loss for 9 days
primary etiology is consumption of alcohol
2.
IVF NS and RL
saline is source of water and electrolytes.It is a crystalloid given intravenously in case of shock, dehydration, and diarrhoea to regenerate the plasma volume.
primary indications for the use of normal saline infusion dehydration, hypovolemia, hemorrhage, sepsis. In metabolic alkalosis in the presence of fluid loss. Mild sodium depletion
Thiamine
Thiamine combines with ATP in the
to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme which participates in many reaction such as in shunt pathway tca etc.
Thiamine hydrochloride injection should be used where rapid restoration of thiamine is necessary, mostly in nerological manifestations
Lorazepam
Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at CNS. It enhances the inhibitory effects of GABA,
indicated in adult patients for preanesthetic medication, producing sedation relief of anxiety.
Pregabalin has anticonvulsant properties. it reduce excitatory neurotransmitter release by binding to the α2-δ protein subunit of voltage-gated calcium channels
Pregabalin is indicated for the managing neuropathic pain. Also in neuropathic pain associated with spinal cord injury
HAI to normalise blood sugar level
Lactulose
Lactulose is used in preventing and treating clinical portal-systemic encephalopathy. It decrease ammoni absorption and productio
KCl
It has many physiological functions.
Maintauning of intracellular tonicity; the transmission of nerve impulses;
Normal renal function
Muscle contraction
Indicated in potassium loss which may be due dehydration fluid loss
3.alcohol withdrawal symptoms
4.thaimine deficiency results in low levels of atp nadph which results in decreased rna production
Also when usual pathway of energy production is halted alternative pathwayresults in excessive accumulation of various metabolites.
5. Mostly due to dehydration
6.Due alcohol consumption which reduces iron absorption
Blood loss becuase of ulcer
7.consulption of alcohol causes peripheral neuropathy here it is due combined affect of diabetic and alcoholic peripheral neuropathy.
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?
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?
1. Giddiness associated with am episode of vomiting 7 days back
Then asymptomatic for the next 3 days
From 2 days he dvloped giddiness associated with aural fullness
bilateral hearing loss
tinnitus
3 of episodes of vomitings
Anatomical localisation duePresence of Infract in the Inferior Cerebellar hemisphere of the Brain
PRIMARY ETIOLOGY: denovo hypertension
Stroke
2.
VERTIN is an anti histamine given to reduce suffering from bi-lateral hearing loss, aural-fullness, tinnitus.
It acts as a agonist on H1 receptors
ZOFER is Ondensetron prevent and traet nausea and vomiting
antagonist of 5HT3 receptors and block ctz pathway
ECOSPRIN is aspirin it has anti platelet function reduces clot formarion
ATORVOSTATIN is a HMG Co A reductase inhibitor in cholestrol synthesis. It decrease s chance of stroke by decreasing vdl and ldl
CLOPIDOGREL antiplatelet function
THIAMINE: to traet neuropathy releated to alcohol
MVT is methylcobalamine given in case of vitamin B12 deficiency
3. Yes.
4.Alcohol consumption lowers the level of fibrinogen, a protein helps in formation of clot. So, there by decreases chance if Ischaemic stroke.
Heavy drinkers have more chance of intra cerebral Haemorrhage
So, in this case, history of alcoholism coupled with effects of hypertension might have resulted in 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?
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?
10 years ago Paralysis of both upper and lower limbs bilateral
1 year ago ight and left paresis
8 months ago Swelling over legs
7 months back - blood infection
2 months back- neck pain
6 days back- pain along left upper limb
5 days back- chest pain, Difficulty in breathing and was able to feel her own heart beat
Anatomical localization: Cervical spine
degenerative changes that occur in the cervical spine is common with age with age.
It results in formation of bone spur as to compensate disc which even disturbs spine
2.
ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression4 in more severe hypokalemia.
3.Cardiology A
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?
2.Why haven't we done pericardiocenetis in this pateint?
3.What are the risk factors for development of heart failure in the patient?
4.What could be the cause for hypotension in this patient?
1.
Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling.
Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure. The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body.
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. As the condition is stable there is not need for pericardiocentesis.
3.
HT
CAD
DM
MEDICATIONS
4 low venous return causes low cardiac output which results in hypotension
B)
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?
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?
4. What sequence of stages of diabetes has been noted in this patient?
1.Hypertension
2.
As co morbid condition of heart failure.
3
diabetes hyperglycemia impairs function of macrophages which results in low immunity
4.
Diabetic microangiopathy and peripheral neuropathy
C
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?
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 is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
4) What are the risk factors for atherosclerosis in this patient?
5) Why was the patient asked to get those APTT, INR tests for review?
1.SOB for last two which progressed from grade II to IV
Oliguria for two days
Anuria since morning
2.
DOBUTAMINE
Acts directly on heart to increase myocardial contraction which causes increase in stroke volume.
Indicated in cardiogenic shock, severe congestive cardiac failure.
UNFRACTIONED HEPARIN it inhibits formation of thrombin. Acts as anti platelet.
Indicatied MI, prophylaxis and treatment of venous thromboembolism, prevention of clotting in arterial and cardiac surgery.
CARVEDILOL
it is a non-selective adrenergic blocker.
Indicated in heart failure with reduced ejection fraction, hypertension, left ventricular dysfunction following MI.
N ACETYLE CYSTEIN increase production of glutathione which acts as antoxidant.
Indicated It is used in paracetamol overdosing, to relive chest congestion due to thickened mucous in cystic fibrosis.
3.
[ ]
Type 4 .
4.
Abnormal lipid profile
Incresed cholesterol
Obesity
5.APTT & INR is indicated to assess the thrombotic activities and complete coagulation profile.
Gastroenterology and pulmonology.
B
) Link to patient details:
https://nehae-logs.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?
2) Name possible reasons why the patient has developed a state of hyperglycemia.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
4) What is the line of treatment in this patient?
1. PLEURAL EFFUSION.
2.hyperglycemia is due to increase in glucagon levels and decrease in insulin
Decresed insulin due to destruction of beta cells of pancreas
Also due to elevated levels of cortisol in stress
3.In liver injury LFT Are ele ated
In which ALT and AST are specific markers for fatty liver.
4
24 hour urinary protein
Fasting and Post prandial Blood glucose
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
5A nephrology
A) Link to patient details:
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
1.what could be the cause for his SOB
compensatoey metabolic acidosis due to diuretic usage
2. Reason for Intermittent Episodes of drowsiness
Decreased sodium levels
3.why did he complaint of fleshy mass like passage inurine
due to infection plenty of pus cell in urine which cause to feell like a flesh mass
4. What are the complicat ions of TURP that he may have had
Turp syndrome
Difficulty micturition
Electrolyte imbalances
Infection
CASE 5B
1.Why is the child excessively hyperactive without much of social etiquettes ?
Attention Deficit Hyperactivity Disorder These include abnormalities in the functioning of neurotransmitters, brain structure and cognitive function.
Low dopamine activity has been associated with the condition,
2. Why doesn't the child have the excessive urge of urination at night time ?
Bcoz ADHD is phycsomatoc disorder.
3. How would you want to manage the patient to relieve him of his symptoms
dopaminergic drugs
6
Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
A) Link to patient details:
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?
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Cough since 2 months on taking food and liquids
•difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
Laryngeal crepitus also favours tracheo oesophageal fistula.
Complications of IRIS can be prevented by careful monitoring the patients with low CD4+ cell count and a thorough history of co-infections. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
7) Infectious disease and Hepatology:
Link to patient details:
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 ?
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 ?
4.What are the indications for ultrasound guided aspiration of liver abscess ?
1. Yes locally made alcohol is contaminated specially toddy
2Alcohol alters permeability of toxins. As in this case absortion of endotoxin increases.
Due to liver damage and unable to detoxify free radicals accentuates the liver abcess
3.
Bcoz right lobe has more blood supply
4.
Indicated when abnormal fluid collection in the patient which can be accessible in various condition such as
Crohn's disease related absces
complicated appendicitis
hepatic absces
retroperitoneal abscess
splenic absces
8
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks
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?
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?
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Diagnosed with hypertension 3 years ago
15 days ago after taking vaccination patient developed fever chill rigor which was subsided by medication
12 days he had similar complaints which was not subsided by medication.
today , patient presented to casualty In altered state with facial puffiness and periorbital edema and weakness of right upper limb and lower limb.
itraconazole antifungal was given as it was the only available drug.
Diabetic ketoacidosis is managed by insulin therapy in addition to it fluid and electrolyte replacement works.
3.
Mucormycosis is may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing.
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