Medicine blended assignment
I have been given the following cases to solve in an attempt to understand the topic of 'patient clinical data analysis 'to develop my competency in reading and comprehending clinical data including history ,clinical findings, investigation and diagnosis and come up with the treatment plan.
This is the link of questions asked regarding the cases
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the medicine assignment based on my comprehension of the cases
PULMONOLOGY
Case 1
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 interms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient problem ?
Ans)Evolution of symptomatology
1st episode of sob - 20 yr back
2nd episode of sob - 12 yr back
From then she has been having yearly episodes for the past 12 yrs
Diagnosed with diabetis - 8yrs back
Anemia and took iron injections - 5yr ago
Generalised weakness - 1 month back
Diagnosed with hypertension - 20 days back
Pedal edema - 15 days back
Facial puffiness- 15 yrs back
Anatomical location of problem - lungs
Primary etiology of patient- usage of chulha since 20 yrs might be due to chronic usage
2)what r the mechanism of action indication and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
Ans)~Head end elevation :# MOA;
. improves oxygenation
.decreases incidence VAP
.increases hemodynamic performance
.increases end expiratory lung volume
.decreases incidence of aspiration
#Indication;.head injury
.meningitis
.pneumonia
~ oxygen inhalation to maintain spo2
~Bipap:non invasive method
#MOA :assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation
(3) Cause for current acute excerbation ?
Ans) it could be due any infection with bacteria or viruses .Typically ,infections cause 75%exacerbations.
(4.) Could the ATT affected her symptoms if so how?
Ans)Yes ATT affected her symptoms
Isoniazid and rifampcin -nephrotoxic - raised RFT was seen
NEUROLOGY
(A.)
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?
Ans) 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 (prefrontal cortex,hypothalamus & limbic system)
Primary etiology :- 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?
Ans) RL & NS :- Electrolyte replenishment
Thiamine :- moa:- combines with ATP in liver , kidney & leucocytes produces thiamine diphosphate which axts as a coenzyme incarbohydrate metabolism in transketolation
Indication :- for low levels of thiamine. For digestive problems (alcoholics have thiamine deficiency)
Lorazepam:- moa :- lorazepam binds to benzodiazepine receptors on postsynaptic GABA-A ligand gated clorine channel neuron at several sites within the CNS. It Inhibits the effects of GABA which increases the conductance of chlorine ions into the cell
Indication :- anxiety disorfers with/ without depression symptoms
Pregabakin :- moa :- it may reduce excitatory neurotransmitter release by binding to the α2-δ protein subunit of voltage-gated calcium channels
(3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier?
What could be a possible cause for this?
Ans) Excessive drinking excites and irritates N.S
Body will be dependent on daily basis for 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?
Ans)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?
Ans) DEHYDRATION
(6). What is the probable cause for the normocytic anemia?
Ans) 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
Ans) yes, it has aggrevated the foot ulcer formation due to anaemia caused by alcoholism
(B)
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?
Ans)giddiness :-7 days back
giddiness after alc 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 (resllved 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?
Ans) Veratin:- moa:- Betahistine is one of the few drugs known which is said to improve the
microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action
(1) agonist of H1 receptors and (2) antagonist of H3 receptors. It has a weak effect on H1 receptors but strong effect on H3 receptors.
Indications:- to prevent diseases of inner ear like menieres disease
Zofer:- moa:- binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea
Ecosprin:- moa :- It irreversibly inhibits prostaglandin H synthase (cyclooxygenase-1) in platelets and megakaryocytes, and thereby blocks the formation of thromboxane A2 .
Atorvostatin :- moa :- 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.
Clopidogrel :- moa :- The active metabolite of clopidogrel selectively 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.
3) Did the patients history of denovo HTN contribute to his current condition?
Ans) Blood vessels damaged by HIGH B.P can narrow,rupture or leak.
High B.P also causes blood clots to form in the arteries leading to the brain,blocking blood flows and potentially causing a stroke.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Ans) Alcohol causes atrial fibrillation leading to stroke.
(C)
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?
Ans) 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?
Ans) 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
Ans) T-wave :- inversion and flattening (mild)
Q-T interval :- prolonged
Visible U wave
(D)
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
- 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
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016826/figure/cells-09-00242-f002/?report=objectonly
• Smoking
• High bloodpressure
• Alcohol
• Obesity
2.what is the reason for anaemia in this case?
Ans) 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?
Ans) 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?
Ans) STAGE 1: insulin resistance
STAGE 2: prediabetes
STAGE 3:diabetes type 2
STAGE4: microvascular complications
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?
A: 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
Rate control - Digoxin, Beta blockers, CCBs like Diltiazem or Verapamil reduce the ventricular rate by slowing AV conduction.
Tab ACITROM -oral anticoagulant used for the treatment and prevention of abnormal clots in blood vessels and diseases associated with it
Thromboprophylaxis - Patients undergoing cardioversion to restore sinus rhythm require temporary anticoagulation to reduce the risk of systemic embolus. Warfarin, direct acting anti-coagulants like factor Xa and direct thrombin inhibitors can be used.
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome in the patient?
Ans)
• 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?
Ans) 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
Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis
3) What are the indications and contraindications for PCI?
Ans)
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?
• Ans) pt experiences many side effects like bleeding,hematoma, and psuedoaneurysm
Overtreatment harms:-
• Increases health care costs
• Psychological and behavioural effects
• Decreases the quality of life
E) 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?
ANS)
• HTN
• DM
• Mild chest pain - 3days back
• Giddiness - since morning
• Profuse sweating - since morning
Anatomical localisation: - B.V
PRIMARY ETIOLOGY:- 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?
Ans) 1.TAB. ASPIRIN
mechanism:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity which helps in PG's production.
Indications: - angina,cardia vadcukar risk,ischaemic stroke
2.TAB ATORVAS
mechanism: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.
Helps in decreasing the bad cholestrol and increasing the good cholestrol
3.TAB CLOPIBB
mechanism:The active metabolite of clopidogrel selectively 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.
Indications :- high risk heart diseases, irregular heart beats
4.INJ HAI
mechanism:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.ANGIOPLASTY
mechanism:Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans) secondary PTCA is not necessary in this patient
Ans) pt has been administered I.V fluids which acted as placebo effect
2. What is the rationale of using torsemide in this patient?
Ans)Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI.
Ans) 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.
Ans:) 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?
Ans: 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
Ans) plueral effusion
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Ans) According to the patient history the he is a chronic alcoholic
alcohol consumption can interfere with blood sugar as well as the hormones needed to maintain healthy blood sugar levels
Chronic alcohol consumption can reduce the overall effectiveness of insulin which results high blood sugar levels ( hyperglycemia)
Hyperglycemia May also be due hypergluconemia secondary to stress
Other reasons for hyperglycemia May arise from mechanism such as uncontrolled pre-existing Diabetes mellitus ,damage to endocrine pancreas to severe attack of acute pancreatitis
3)What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Ans) Elevated liver function test especially ALT and Bilirubin level may be suggestive of CHOLIDOCHOLITHIASIS (Gallstones in common bile duct)
LFT are increased due to hepatocyte injury
Biochemical markers for chronic alcohol consumption that have been most commonly studied are serum GGT
elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
4)line of treatment in this patient?
Ans) Supportive therapy like IV Fluids to prevent dehydration
GRBSmonitoring
Analgesics to relieve pain
Antiemetics and treatment of underlying cause and treatment for alcohol dependence
1) What is the most probable diagnosis in this patient?
Ans) Differential Diagnosis:
· Ruptured Liver Abscess.
· Organized collection secondary to Hollow viscous Perforation.
· Organized Intraperitoneal Hematoma.
· Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
· Grade 3 RPD of right Kidney
The most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.
2) What was the cause of her death?
Ans) After leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.
3) Does her NSAID abuse have something to do with her condition? How?
Ans) NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure.
1.what could be the cause for his SOB
Ans) His sob was is due to Acidosis which was caused by Diuretics
2. Reason for Intermittent Episodes of drowsiness
Ans) Hyponatremia was the cause for his drowsiness
3.why did he complaint of fleshy mass like passage inurine
Ans) plenty of pus cells in his urine passage appeared as
fleshy mass like passage to him
4. What are the complications of TURP that he may have had
Ans) Difficulty micturition
Electrolyte imbalances
Infection
Ans) 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 ?
Ans) 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?
Ans) 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.
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.
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
Ans) Cough since 2 months on taking food and liquids (which was initially non productive then associated with sputum which is white in color , moderate in quantity and non foul smelling)
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Ans) IRIS OCCURS IN 2 forms
Patients with mycobacterial disease at the time of initiation of ART are at higher risk of developing 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.
7) INFECTIOUS DISEASES AND HEPATOLOGY
1) Cause of liver abcess in this patient ?
Ans) If the cause is infectious, the majority of liver abscesses can be classified into bacterial (including amebic) and parasitic sources (including hydatiform cyst)
Amoebic liver abscess is an important cause of space-occupying lesions of the liver; mainly in developing countries
Most amoebic infections are caused by Entamoeba histolytica consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.
2) How do you approach this patient?
A) Considering the following factors:
1) Age and gender of patient: 21 years ( young ) and male.
2) Single abcess.
3) Right lobe involvement.
The abcess is most likely AMOEBIC LIVER ABSCESS …
But most of the patients with amoebic liver abcess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and insensitive and not recommended.
Ans) Serologic testing is the most widely used method of diagnosis for amebic liver absces
In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease)
