Monday, 31 May 2021

Online blended bimonthly assignment

 Online blended bimonthly assignment toward summative assessment for the month of May 2021

D. THANMAI

ROLL NO: 27

2017 BATCH                                                                                                   31 MAY 2021

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.





                                                              1.PULMONOLOGY 

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

1. a) Bacterial or allergens exposure in paddy fields caused  shortness of breath leading to  increase in load on right heart causing right heart failure which lead to pedal edema and puffiness of face 

b) anatomical localization of problem - Bronchi 

c) Constant exposure to Allergens or bacteria ,weak immunity 

2. a HEAD END ELEVATION:

 MECHANISM OF ACTION: 
→Improves oxygenation.
→Decreases incidence VAP
→   Increase hemodynamic performance   ✓Increase end expiratory Lung volume
→ Decrease incidence of aspiration
   
INDICATIONS:
 Meningitis, Head injury, Pneumonia 
b.OXYGEN INHALATION TO MAINTAIN SPO2 ABOVE 92%

c.BiPAP : assist ventilation  by delivering positive expiratory and inspiratory pressure with out need for Endo Tracheal incubation

d.AUGMENTIN (Amoxicillin,clavulinic acid)

Mechanism of Action
Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes.

e. AZITHROMYCIN

Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit.

f.LASIX( FUROSEMIDE)

Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine.

g.HYDROCORTISONE.

Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.

h.IPRAVENT:

Ipravent  work by relaxing the bronchial tubes (air passages) that carry air in and out of your lungs. This makes breathing less difficult.

i.PANTOP (PANTAPRAZOLE)

  pantoprazole inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.

3. current acute exacerbation may be due to 

ATT drugs causing weakness or upper respiratory tract infection

4. yes, it effected by causing generalized weakness 

5. could be due to renal insufficiency ,hypoxia , hypercapnia ,respiratory acidosis etc


                                                            2.NEUROLOGY

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

A.

1. a.2 years ago patient is diagnosed with Diabetes type II → he did not follow anti diabetic treatment →  year ago severity increased → 4 months ago he developed seizure following sesation of alochol after 24 hrs → 10 days ago he developed general body pains →9 days ago he developed altered sensorium such as irrelevant talking and decreased food intake.

b.Central nervous system 

c. ETIOLOGY Prolonged alcohol use leads to the development of tolerance and physical dependence, which may result from compensatory functional changes by downregulation of GABA receptors and increased expression of NMDA receptors with production of more glutamate to maintain central nervous system (CNS) transmitter homeostasis

Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate-mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures.The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits.


2 

a. IVF NS and RL 

 mechanism:Administer intravenous (IV) fluids for rehydration, as necessary. Most patients with severe alcohol withdrawal are significantly dehydrated, and their fluid requirements range from 4-10 L in the first 24 hours. Because hypoglycemia is common in these patients due to depleted glycogen stores, a 5% dextrose solution (in 0.90% or 0.45% saline) should be used to prevent hypoglycemia.

b. Inj. THIAMINE 
mechanism:
*
  • It is well known that chronic alcoholics are at high risk for being deficient in vitamin B1 (thiamine), which is known to put the patient at an increased risk for Wernicke-Korsakoff Syndrome, cerebellar degeneration, and cardiovascular dysfunction.
  • What does thiamine contribute that allows the cells in the brain to respond to this metabolic demand?
    Upon absorption into the body, thiamine is used to form thiamine pyrophosphate, which is an essential co-factor used by several cellular enzymes.



c. Inj. Lorazepam
mechanism:Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell.

d. T. Pregabalin 
mechanism: Pregabalin is structurally related to the antiepileptic drug gabapentin and the site of action of both drugs is similar, the alpha2-delta (alpha2-delta) protein, an auxiliary subunit of voltage-gated calcium channels. Pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions in vivo to reduce neuronal excitability and seizures.

e. Inj. HAI S.C.- premeal
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

f. GRBS 
mechanism:Regular blood glucose monitoring is an essential tool to help you take control of your diabetes. By identifying and recording changes in your blood sugar levels, you'll have more information about how food, exercise, stress, and other factors affect your diabetes.

g. glucose monitoring
mechanism:Regular blood glucose monitoring is an essential tool to help you take control of your diabetes. By identifying and recording changes in your blood sugar levels, you'll have more information about how food, exercise, stress, and other factors affect your diabetes.

g. Inj  ampoule KCl 
mechanism:Potassium ions participate in a number of essential physiological processes, including the maintenance of intracellular tonicity; the transmission of nerve impulses; the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of normal renal function.

h. Syp Potchlor 
mechanism:It helps to maintain potassium balance in the body by restoring normal potassium levels in patients with a low level of potassium.

3.Long-term abuse can damage the nervous system liver and other organs this damage maybe is reversible drinking too much alcohol can also alter the level of certain nutrients in the body including
* thiamine
* folate
* vitamin B6 and B 12
vitamins are needed for proper no function and can also cause alcohol related neurological diseases.

4.  thiamine is given to patient because it forms thiamine pyrophosphate which is essential for cycles to generate ATP

5. Sudden withdrawal of alcohol cause injury to kidney 

6.  Sudden withdrawal of alcohol cause injury to kidney thus causing normocytic anemia 

7. excessive alcohol intake caused poor wound healing in this patient thus leading to ulcer'



B.

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

1. a.no Slurring of speech, deviation of mouth that got resolved the same day

b. infarct in the inferior cerebellar hemisphere of the brain.

c.In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.

2. PHARMACOLOGICAL INNTERVENTIONS

1)Tab Veratin 

MECHANISM:

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.


2)Inj Zofer 

MECHANISM:

Zofer Tablet works by inhibiting the action of a chemical substance named serotonin, which is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea.


3)Tab Ecosprin 

MECHANISM:

Ecosprin is an antiplatelet medicine. It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot.


4)Tab Atorvostatin

MECHANISM:

Atorvastatin is in a class of medications called HMG-CoA reductase inhibitors (statins). It works by slowing the production of cholesterol in the body to decrease the amount of cholesterol that may build up on the walls of the arteries and block blood flow to the heart, brain, and other parts of the body.


5)Tab Clopidogrel 

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.


6)Inj Thiamine

MECHANISM:

Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.


3.  yes, HTN caused stroke by formation of artero sclerosis in cerebral arteries 

4. yes, alcohol consumption cause decreased liver protiens that helps in clot formation. thus it increases risk for stroke due to bleeding  



C.


1. a. patient was normal 8 months back then developed b/l pedal edema which gradually progressed.

Aggerevated in sitting and standing position, relived on taking medication
*Palpitations :since 5days, sudden in onset which is more during night
Aggerevated by lifting heavy weights, speaking continuously
*Dyspnoea during palpitations since 5 days
*pain:since 6days, radiating along left upper limb, more during palpitations and relived on medication.
Chest pain associated with chest heaviness since 5 days.
ETIOLOGICAL AGENT:
*By localization, electrolyte imbalance (hypokalemia) causing the her   manifestations like palpitations, chest heaviness, generalised body weak   ness
*radiating pain along her left upper limb due to cervical spondylosis.

2. Diuretics 

3.Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves 

symptoms of hypokalemia:
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.


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

D.

1. If you've had a stroke, you have an increased risk for having a seizure. A stroke causes your brain to become injured. The injury to your brain results in the formation of scar tissue, which affects the electrical activity in your brain. Disrupting the electrical activity can cause you to have a seizure.

2.Abnormal increased activity in fronto-parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures. Abnormal decreased activity in these same networks may cause loss of consciousness in complex partial seizures.



E. 

1.→Addicted to alcohol for the past 3 years. According to the attendant he used to drink "a few bottles per day". Drinks both bottled liquor and toddy. 

→History of multiple falls when inebriated and history of minor head injuries that were left unattended.
→History of change in gait since 1 year
→The CT scan showed an acute cerebral hemorrhage of the frontal, parietal and temporal lobes with a 13mm midline shift.

So, Alcohol might be responsible for his present condition.

2. Alcohol-induced impairment of the blood-clotting and/or fibrinolytic systems can have serious medical consequences. Most significantly, clinical epidemiological data suggest that a recent bout of heavy drinking increases the drinker’s risk of suffering a hemorrhagic or ischemic stroke. During a hemorrhagic stroke, the blood flow to a brain area is impaired due to a ruptured blood vessel that results in bleeding in the brain. If the blood flow is interrupted because a blood vessel is blocked by a blood clot.


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

F.

1. since patient doesn't have diabetes or hypertension RTA could possibly be the cause for his present condition  

2.

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

Sudden confusion, trouble speaking, or difficulty understanding speech.

  • Sudden trouble seeing in one or both eyes.

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

3.

Aspirin -antiplatlet drug prevents stroke

Atorvostatin - decreases LDL cholesterol to prevent recurrent attacks of stroke.

4.in this case alcohol does not play a major role in cva as he drinks alcohol ocassionally.

5. No, his lipid profile is in normal range




G.

1. 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.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.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.

1. According to MRI  cortical vein thrombosis might be the cause of her seizures.

2.

  • Pregnancy and the first few weeks after delivery
  • Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation
  • Cancer
  • Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
  • Obesity
  • Low blood pressure in the brain (intracranial hypotension)
  • Inflammatory bowel disease like Crohn’s disease or ulcerative colitis

3.there was a sezuire free period due to administration of antiepileptic drugs as the effect of drugs weans off the sezures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the sezuires.

4.heparin as CLEXANE was given to relive clot in suspission of CVST


                                                                 3.CARDIOLOGY

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

A.

1.

2. As there is risk for lung injury pleural tap has been avoided

3. risks for developing heart failure could be pericardial effusion could lead to cardiac tamponade causing heart failure ,known case of AV block

4. hypotension is due to pericardial effusion 


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

B.

1. hypertension→ left ventricular hypertrophy ,uncontrolled hyperglycemia ,obesity

2. Anemia due to chronic illness

3. (GRBS - 290% ) non healing ulcers due to un controlled diabetes 

4. initially patient was diagnosed with type 2 Diabetes , he was prescribed with oral hyperglycemic drugs ,the he was prescribed with insulin later it progressed to stage 4 where he faced vascular complications such as retinopathy the micro vascular complications such as non healing ulcers.


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

C.  

1. a. 10 years ago patient has undergone surgery for  inguinal herina → 3 yyears ago he has a history of NSAID abuse andon and off  facial puffines → facial puffiness prolonged for next 2 years →1 year ago he developed grade II SOB and HTN →2 days ago he has decreased urine out put + SOB grade II  which progressed to grade IV 

b. Anatomical localization : Blood vessels 

c.The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.

The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.

2. PHARMACOLOGICAL INTERVENTIONS


a. TAB. Dytor
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
b.TAB. Acitrom 
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
c. TAB. Cardivas 
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
d. INJ. HAI S/C
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
e.TAB. Digoxin 
mechanism:
Digoxin has two principal mechanisms of action which are selectively employed depending on the indication: Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,
an enzyme that controls the movement of ions into the heart.
f. Hypoglycemia symptoms explained
g. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
h. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

3. this patient have cardio renal syndrome type IV 

PATHOGENESIS OF CARDIO RENAL SYNDROME IS DEPECITED IN THE BELOW FIGURE


4.  Hypertension

5. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.


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

1.TIMELINE OF EVENTS-

 Diabetes since 12 years - on medication
Heart burn like episodes since an year- relieved without medication
Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
Hypertension since 6 months - on medication
Shortness of breath since half an hour-SOB even at rest

Anatomical localisation - Cardiovascular system
Etiology:  The patient is both Hypertensive and diabetic , both these conditions can cause
                  - Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)

2.PHARMACOLOGICAL INTERVENTIONS

  • Met XL 
   MECHANISM: Tablet belongs to a group of medicines called long-acting beta-blocker. Met XL  Tablet works by  blocking the effects of some chemicals on your heart and blood vessels. It slows down  your heart rate and helps it to beat with less force
  • 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     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. Provider-related factors

  • Inappropriate PCI recommendation without coronary artery bypass grafting (CABG) facility availability.

  • PCI and diagnostic catheterisation performed during the same session (ad hoc PCI).

  • Lack of shared decision making.

  • Medico-legal concerns related to risks from failed medical intervention.

  • Poorly regulated, privatisation and fee-for-service in healthcare.

  • Fear of missing the ‘widow-maker’.

Patient related factors

  • Patient preference for minimally invasive PCI over CABG.

  • Lack of health literacy among patients.

  • Fear, anxiety, misperceptions and misbeliefs among patients about PCI benefits over optimal medical therapy and lifestyle modification.




E
1. a. 3 days ago chest pain which is insidious , gradual and dragging type →giddiness and profuse sweating 
b.Anatomical location : Blood vessels 
c.Etiology myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function

2. PHARMACOLOGICAL INNTERVENTION


a.TAB. ASPIRIN
mechanism:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.

b.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.

c.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.

d.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

d.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.
PCI in this patient is not necessary because
Primary PCI is only indicated when symptoms duration is 12-24 hours (delayed presentation) if severe congestive heart failure, hemodynamic/electrical instability or continued angina is present. Primary PCI is not recommended when symptom onset is more than 12 hours and the patient is asymptomatic (OAT trial).




https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h

F

1.Because of the  fluid loss occurred to the patientthere is decreased preload- so, SOB occurred due to decreased CO

IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.

2.Torsemide used to relieve abdominal distension 

3.IT IS THE TREATMENT FOR UTI
 Rationale- Used for any bacterial infection.



4.GASTEROENTEROLOGY & PULMONOLOGY 


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

A

1.Evolution of symptomatology 

H5 years back-1st episode of pain abdomen and vomitings 
Stopped taking alcohol for 3 years
1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again 
20 days back increased consumption of toddy intake
Since 1 week pain abdomen and vomiting
Since 4 days fever constipation and burning micturition

Antomical location of etiology is pancreas(ductal obstruction, acinar cell injury, defective intracellular transport)


The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes     Attributed to alcohol

2.PHARMACOLOGICAL INTERVENTIONS

a. ING. MEROPENAM 

mechanism:Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.

b. ING. METROGYL 

mechanism:Metronidazole diffuses into the organism, inhibits protein synthesis by interacting with DNA and causing a loss of helical DNA structure and strand breakage. Therefore, it causes cell death in susceptible organisms.

c. ING. AMIKACIN 

mechanism:he primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.

d. TPN ( Total Parenteral Nutrition )

mechanism: the early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infectionTPN is only required in a few patients.

e. IV NS / RL 

mechanism:Patients with acute pancreatitis lose a large amount of fluids to third spacing into the retroperitoneum and intra-abdominal areas. Accordingly, they require prompt intravenous (IV) hydration within the first 24 hours. Especially in the early phase of the illness, aggressive fluid resuscitation is critically important.

f. ING. OCTREOTIDE 

mechanism:

Like somatostatin, octreotide also decreases the release of growth stimulating hormones, decreases blood flow to the digestive organs, and inhibits the release of digestive hormones such as serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide.

Octreotide is useful in overdose management of sulfonylurea type hypoglycemic medications, when recurrent or refractory to parenteral dextrose. Mechanism of action is the suppression of insulin secretion.

g. ING. PANTOP 

mechanism:The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.

h. ING. THIAMINE

mechanism:Vitamin B1 (thiamin) is indispensable for normal function/health of pancreatic cells due to its critical role in oxidative energy metabolism, ATP production, and in maintaining normal cellular redox state.

i. ING. TRAMADOL 

mechanism:Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.




B.  
1.the cause of dyspnea might be PLEURAL EFFUSION.

2.This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
 the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells 
 elevated levels of catecholamines and cortisol.

3.reason for his elevated LFT is heaptocyte injury 
specific markers for alcoholic fatty liver disease are ALT and AST 

4.Investigations:
 24 hour urinary protein 
Fasting and Post prandial Blood glucose
HbA1c
USG guided pleural tapping 
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 



 
C.
1. haemoperitonium
2.blood loss due to haemoperitonium leading to shock
3. her  NSAID abuse might have caused drug induced hepatitis which in turn lead to cirrhosis  




                                     5) Nephrology (and Urology) 

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

A.  

1the reason for SOB was- metabolic acidosis .

2.   He has intermittent episodes of drowsiness because of increased levels of creatinine in the body...

When the creatinine quantity decreased to normal level the patient the patient become allright....
But again when the creatinine levels raises the patient becomes drowsy.

3. He complains of fleshy mass in urine because of patient feels thick urine coming out of his body...the reason behind is the patient had urosepsis.....the culture and sensitivity showed the E.Coli infection...it is the most common cause of UTI....because these infection many pus cells has formed...and these pus cells increase the cloudyness of the urine ..so the patient feels fleshy mass like urine.

4..INTRA-OPERATIVE COMPLICATIONS 1-Hypotension 2-TURP syndrome 3-Haemorrhage 4-Perforation of bladder/prostatic capsule 5-Hypothermia 6-Bacteremia and sepsis 7-Complications of positioning 8-Erection.


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


B.

1.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. the child doesn’t have the excessive urge of urination at night time because ADHD is a physcosomatic disorder 

3.



6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)

A) 1. cough on taking food , liquids and difficulty in swallowing suggests tracheoesophageal fistula
     
2. immune reconstitution inflammatory syndrome (IRIS) develops in patients who are on ART since this patient is on ART he might develop IRIS . to prevent this ART must me initiated before the  development of advanced immunosuppression.


7) Infectious disease and Hepatology 
   

A) 1.  d1. Amoebic liver abscess (ALA) is the most common manifestation of invasive amoebiasis caused by Entamoeba histolytica (EH). Several studies from India have reported a strong link between consumption of toddy and the occurrences of ALA. Toddy

 2. Pathophysiology
Infection can reach the liver in several ways (Box 22.43). Pyogenic 
abscesses are most common in older patients and usually result 
from ascending infection due to biliary obstruction (cholangitis) or 
contiguous spread from an empyema of the gallbladder. They can 
also complicate dental sepsis or colonic pathology, e.g. cancer, 
diverticulitis or inflammatory bowel disease causing portal pyaemia.

 3. Right lobe receives blood from
     Superior mesenteric and PORTAL VEINS
   *STREAMING EFFECT IN PORTAL CIRCULATION IS CAUSATIVE

 4. INDICATIONS OF LIVER ABSCESS DRAINAGE:

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

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

c) If the abscess is not responding to the drugs for 7 or more days.





B) 1. cause of liver abscess in this patient is due to Entamoeba hystolytica infection

     2.

     3. we treat the patient for both amoebic and pyogenic abscess  so that we don't rely only on anti-amebic therapy and insure complete treatment of the cause
     4. confirmatory test for amoebic abscess is
Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extra intestinal disease).

The diagnosis of amoebic liver abscess was based on four or more of the following criteria:
 (i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess, 
(ii) clinical symptoms (fever, pain in the right hypochondriac (often referred to the epigastrium), lower chest, back, or tip of the right shoulder), 
(iii) enlarged and/or tender liver, usually without jaundice, 
(iv) raised right dome of the diaphragm on chest radiograph, and 
(v) improvement after treatment with anti amoebic drugs (e.g., metronidazole). 

 

8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

A) 1. 3 years back HYPERTENSION  →  on 18th April 2021[ he took COVID-19 Vaccine  → developed high grade fever with chills and rigor  → relieved on medication  ]→ 3 days later similar symptoms which did not relieved on medication  →on 18th April 2021[ generalized weakness, facial puffiness, peri orbital edema and drowsiness ] → 4th May 2021 [facial puffiness , peri orbital edema , weakness of upper and lower limbs ]

 2.  Itraconazole acts by inhibiting the fungal cytochrome P-450 dependent enzyme lanosterol 14-α-demethylase. When this enzyme is inhibited it blocks the conversion of lanosterol to ergosterol, which disrupts fungal cell membrane synthesis.

Amphotericin B binds with ergosterol, a component of fungal cell membranes, forming pores that cause rapid leakage of monovalent ions (K+, Na+, H+ and Cl) and subsequent fungal cell death

 3.  un regulated usage of steroids in COVID-19 effected patients who are also having co morbidities like Diabetes ,show rise in the incidence of Mucormycosis 


9) http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1

10) I personally would love to learn without stress ,without rushing and with in depth info . I felt link there is more to learn .

A 55 YEAR OLD MALE WITH PAIN ABDOMEN

C/C ABDOMINAL PAIN SINCE 6.PM ON 8/12/2022 VOMITINGS - 5 EPISODES SINCE MORNING (NON PROJECTILE) HOPI:  PATIENT WAS APPARENTLY NORMAL TILL T...