MEDICINE BLENDED ASSAIGNMENT

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

1A)Myelopathy hand-loss of power of adduction and extension of ulnar two or three finger and an inability to grip and release rapidly with these fingers .These changes are termed as 'myelopathy hand'         it is due to pyramidal tract involvement.


Severe cervical flexion myelopathy with long tract signs: a case report and  a review of literature | Spinal Cord Series and Cases


2a)it is also known as Wartenberg sign is a neurological sigh of involuntary abduction of little finger caused by unopposed action extensor digiti minimi .It is seen in cervical myelopathy.

3A)Hoffman reflex -it is a neurological examination finding elicited by reflex test which can help to verify the presence or absence of issue arising from corticospinal tract.

Clinical Correlations of Cervical Myelopathy and the Hoffmann Sign in:  Journal of Neurosurgery: Spine Volume 9 Issue 3 (2008)

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

1A)Yes, the history of RTA may play role in present condition . Which may be the cause for infract in left middle cranial artery territory. Which led to decrease supply to left internal capsule, caudate, putamen, left thalamus, left insular lobe.

2A)  1.Sudden onset of weakness or numbness on one side of body.                                                                     2.sudden speech difficulty or confusion.                                                                                                      3.sudden difficult in seeing in one or both eye.                                                                                            4.sudden severe headache.                                                                                                                              5.loss of balance, difficulty in walking, dizziness.                                                                                  

 3A)tissue plasminogen activator- alteplase, tenecteplase- break down of clot                                                   mannitol-to lower ICP                                                                                                                                  aspirin-COX inhibitor-to make blood thin                                                                                                     atovarstatin-decrease LDL and increase HDL 

4A)Alcohol consumption has no role in development of CVA as patient consume alcohol occasionally .

5A)HDL-absorb cholesterol and carry back to liver where the liver flushes out cholesterol from body .         high level of HDL decrease the risk of heart diseases.


1A)After stroke there is increased risk of seizures                                                                                              after injury there is scar formation which affect the electrical activity in brain cause decrease in                electrical activity which lead to seizure.                                                                                                         people with hemorrhagic shock more likely to have seizures after stroke compared to those having          ischemic stroke.
2A)It may be due to scar formation lead to worsening of symptoms. Abnormal activity in fronto parietal        association cortical area.      


1A)Alcohol may be the cause of Ataxia casing cerebellar degeneration.(ALCOHOL INDUCED                    ATAXIA)
2A)Multiple falls may be the cause of intra cranial bleeding. Alcohol consumption has no advantages i          increase in alcohol consumption lead to increase B.P which may lead to increase in intra cranial               bleeding.


1A)IRON DEFICIENCY ANEMIA may be cause of her condition

                                    

 2a)Risk factors for cortical vein thrombosis:
      sickle cell anemia
      chronic hemolytic anemia
      beta thalassemia   
      iron deficiency anemia
      heart diseases 
      dehydration.

  3A)there was a seizure free period due to administration of antiepileptic drugs as the effect of drugs weans off the seizures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the seizures.
  
4A)anticoagulant- low molecular weight heparin-I.V
  thrombolytic drugs
  antihypertensive drugs
  antiepileptic drugs.

  https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

1A)pleural effusion might be the cause of dyspnea.                                                                                          relation of effusion and pancreatitis:

      increase permeability of lymphatics may lead to shift of pancreatic enzymes from abdomen to                  thorax. impairment of drainage of pleural exudate caused by lymphatic obstruction. increase in                 permeability of diaphragm lead to inflammation of adjacent pancreas.

2A)hyperglycemia may be caused due to decrease synthesis of insulin which is damage of beeta cells of pancreas in acute pancreatitis.

3A)LFT is elevated due to HEPATIC CELL DAMAGE                                                                              if there is liver damage there is increase level ALT level in our body                                                     *ALT and AST are specific marker for Alcoholic Fatty Liver Disease.

4a)Plan of action and Treatment:

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 

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

1a)HEMOPERITONIUM might be the probable diagnosis

2A)In hemoperitonium the blood accumulate in various abdominal cavities . which lead to decrease perfusion to various organs which lead to shock and finally death.

3a)NSAIDS intake for long duration may lead to drug induced hepatitis                                                                

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

1A)cause of SOB-METABOLIC ACIDOSIS                                                                                                    metabolic acidosis in kidney disease may lead to:                                                                                          *impaired ammonia excretion                                                                                                  * reduced tubular bicarbonate reabsorption                                                                             * insufficient renal bicarbonate production 

2A)metabolic acidosis cause fatigue by inhibition of release of ca+2 from SR which decrease the activity of muscle contraction.

3a)the cause of fleshy mass  in urine might be due to papillary necrosis following hydronephrosis

4a)after TURP surgery there might be urethral stenosis which cause backflow of urine which lead Hydronephrosis and to papillary necrosis.

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

1a)it is due to ATTENTION DEFECIT HYPERACTIVE DISORDER(ADHD)
                        

                
                                                                                                                                                                         2a)As ADHD is psychological disorder  the patient has urge of urination when he is awake only.

  


3a) Evaluation and Treatment of ADHD in Children and Adolescents*

                                                                                                                                                                     

https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html


1a)Infants may develop rattling respiration and episodes of coughing and choking in association with cyanosis. Symptoms worsen during feeding in the presence of a tracheoesophageal fistula (TEF). The symptoms induced by malignant TEFs are cough, aspiration (especially on swallowing liquids), and fever.


2a)Immune reconstitution inflammatory syndrome (IRIS) occurs in two forms: "unmasking" IRIS refers to the flare-up of an underlying, previously undiagnosed infection soon after antiretroviral therapy (ART) is started; 
"paradoxical" IRIS refers to the worsening of a previously treated infection after ART is started.
                                                                                                                                                   

How can immune reconstitution inflammatory syndrome be prevented?

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.


https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html


1a)yes, drinking locally made alcohol cause liver abscess in this patient due to predisposing factors for the formation of liver abscess both amoebic and pathogenic liver abscess

2a)It is unknown why most amoebic liver abscess (ALA) cases occur in alcohol drinkers. In experimental studies, the presence of 'iron' potentiates the in-vitro growth of Entamoeba histolytica (E. histolytica), and is also known to increase its in-vivo invasiveness in animal infections. 
 Chronic alcoholism increases the hepatic iron deposition. We hypothesized that ALA occurs more commonly in livers with a high iron load as in alcoholics. To test this hypothesis we compared the levels of iron between ALA and non-ALA cases belonging to alcoholic and non-alcoholic groups.

3a)


4a) The indications for drainage of amebic liver abscess include the following:
 1A)
  • Stage 1 -- Mild -- FEV-1 ≥80%: You may have no symptoms. You might be short of breath when walking fast on level ground or climbing a slight hill.
  • Stage 2 -- Moderate -- FEV-1 50-79%: If you’re walking on level ground, you might have to stop every ­few minutes to catch your breath.
  • Stage 3 -- Severe -- FEV-1 30-49%: You may be too short of breath to leave the house. You might get breathless doing something as simple as dressing and undressing.
  • Stage 4 -- Very Severe -- FEV-1 ≤30%: You might have lung or heart failure. This can make it hard to catch your breath even when you’re resting. You might hear this called end-stage COPD.
  • anatomical localization of disease in patient is BRONCHIOLE
  • Primary etiology of COPD  in this patient is exposure to PADDY FOR LONG DURATION. 

2a)
Treatment
           

  • Quitting smoking

The most essential step in any treatment plan for COPD is to quit all smoking. Stopping smoking can keep COPD from getting worse and reducing your ability to breathe.                        

Bronchodilator

Bronchodilators are medications that usually come in inhalers — they relax the muscles around your airways. This can help relieve coughing and shortness of breath and make breathing easier. xamples of short-acting bronchodilators include:

  • Albuterol (ProAir HFA, Ventolin HFA, others)
  • Ipratropium (Atrovent HFA)
  • Levalbuterol (Xopenex)

Examples of long-acting bronchodilators include:

  • Aclidinium (Tudorza Pressair)
  • Arformoterol (Brovana)
  • Formoterol (Perforomist)
  • Indacaterol (Arcapta Neoinhaler)
  • Tiotropium (Spiriva)
  • Salmeterol (Serevent)
  • Umeclidinium (Incruse Ellipta)

Inhaled steroids

Inhaled corticosteroid medications can reduce airway inflammation and help prevent exacerbations. Side effects may include bruising, oral infections and hoarseness. These medications are useful for people with frequent exacerbations of COPD. Examples of inhaled steroids include:

  • Fluticasone (Flovent HFA)
  • Budesonide (Pulmicort Flexhaler)

Combination inhalers

Some medications combine bronchodilators and inhaled steroids. Examples of these combination inhalers include:

  • Fluticasone and vilanterol (Breo Ellipta)
  • Fluticasone, umeclidinium and vilanterol (Trelegy Ellipta)
  • Formoterol and budesonide (Symbicort)
  • Salmeterol and fluticasone (Advair HFA, AirDuo Digihaler, others)

Phosphodiesterase-4 inhibitors

A medication approved for people with severe COPD and symptoms of chronic bronchitis is roflumilast (Daliresp), a phosphodiesterase-4 inhibitor. This drug decreases airway inflammation and relaxes the airways. Common side effects include diarrhea and weight loss.

Antibiotics

Respiratory infections, such as acute bronchitis, pneumonia and influenza, can aggravate COPD symptoms. Antibiotics help treat episodes of worsening COPD, but they aren't generally recommended for prevention. Some studies show that certain antibiotics, such as azithromycin (Zithromax), prevent episodes of worsening COPD, but side effects and antibiotic resistance may limit their use.

3a)cause of acute exacerbation might be                                                                                    upper respiratory tract infection  and allergen exposure(paddy)  

4a)ATT could have effected the patient’s condition by causing generalised weakness.

5a) Hyponatremia in patients with COPD developed secondary to many reasons, such as development or worsening of hypoxia, hypercapnia, and respiratory acidosis, and right-side heart failure with development of lower limb edema, renal insufficiency, use of diuretics, Syndrome of Inappropriate Antidiuretic Hormone Synthesis, malnutrition, and poor intake during acute exacerbations are common contributing factors in such patients  .                             Moreover, respiratory acidosis with metabolic alkalosis (owing to renal compensation) in patients with COPD with chronic hypercapnia is the usual cause of hypochloremia in those patients. So, patients with severe COPD exacerbation have factors that influence serum electrolytes levels like hypoxia, respiratory acidosis, and hypervolemia, even before starting any type of treatment that may further cause electrolyte imbalance                                                                                                    


1A)
  • history of giddiness 7 days back. It started at around 7 am when the patient was doing his usual morning routine. He suddenly felt giddy and took rest, after which it subsided briefly. This was associated with 1 episode of vomiting on the same day.
  • - Patient was asymptomatic for 3 days, after which he consumed a small amount of alcohol.
  • - He then developed giddiness, that was sudden in onset, continuous and gradually progressive. It increased in severity upon getting up from the bed and while walking.
  • - This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.
  • - He has associated vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.
  • - Patient has H/o postural instability- he is unable to walk without presence of supports, swaying is present and he has tendency to fall while walking                                                         
  • anatomical localization is CEREBRAL BLOOD VESSELS
  • DENOVO HTN is primary etiology of this problem. 

2a)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 Zofe

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.


3a)yes, the patients history of denovo HTN contribute to his current condition                                                    Hypertension induces structural and functional alterations in cerebral blood vessels, which compromise the blood supply to the brain and increase the risk of stroke and dementia.

4a)Liver damage due to too much alcohol can stop the liver from making substances that help your blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.


https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

1a)cause of liver abscess might be due to toddy which was contaminated.
histolytica infection induces apoptosis in hepatocytes in amebic liver abscess. Apoptosis occurs in hepatocytes and inflammatory cells in amebic liver abscesses in SCID, C57BL/6.

2A)Use the amebicidal drugs is the first line treatment of amebic liver abscess. Metronidazeole is the drug of choice. The size of the abscess is an important factor in determining the response to medical treatment. Percutaneous needle aspiration and/or catheter drainage are the other modalities of treatment.

3a)# The abcess is most likely to be AMOEBIC LIVER ABCESS. 

* Since we cannot take risk , we should however administer antibiotics also ( like in pyogenic liver abcess)

* INJECTION. ZOSTUM 1.5 gm IV BD (twice daily) 

 Zostum is a  combination of  drugs - SULBACTUM (pencillin) & CEFOPERAZONE(cephalosporin) [Antibiotic]: It is used here to treat if any bacterial cause ( since we can’t take the risk relying on only anti amoebic therapy) 

* INJECTION. METROGYL 500mg IV TID ( thrice daily )

Metrogyl has the drug called METRONIDAZOLE [Antibiotic]: For amoebic cause 

* INJECTION. OPTINEURIN 1amp in 100 ml NS( Nor

mal Saline) IV OD ( once daily)

Optineurin is a multivitamin drug { A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement 

* TAB. ULTRACET 1/2 QID( four times a day)

Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and fever 

* TAB. DOLO 650 mg SOS (if needed) given for fever and pain 

* Here ; due to medical therapy his symptoms subsided and clearly we can see it in usg reports ( liquefaction) meaning abcess responded to our medical therapy. 

*And the patient was discharged on 10/5/21.

* We donot aspirate the pus since it is self resolving and aspiration is associated with several other complications.

* However there are some important indications for draining the abcess often asked in exams.

4a)diagnosis of pyogenic liver abscess

  • an abdominal ultrasound to locate an abscess
  • CT scan with intravenous contrast, or injected dye, to find and measure the abscess
  • blood tests to look for signs of infectious inflammation, such as an increased serum white blood count and neutrophil level
  • blood cultures for bacterial growth to determine which antibiotic(s) you need an MRI of the abdomen

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

1a)Patient was apparently asymptomatic 3 years back and went to local hospital in/v/o Regular checkup and came to diagnosed with Hypertension since then he was on regulate medication..

                                                         //
And on 18/04/21 He went to local PHC for COVID 19 vaccination.. Since that night patient is complaining of Fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication... 
                                                        //
Followed by patient is having similar complaints after three days and he visited local hospital which is not subsided by medication ( Antipyretics) ( not taken medication such as steroids, oxygen therapy, anti virals) 
                                                     //
On 28/04/21 , c/o Generalized weakness and facial puffiness and periorbital edema.. And also patient is in drowsy state.. 
                                                    //
 On 04/05/21, patient presented to casualty In altered state with facial puffiness and periorbital edema and weakness of right upper limb and lower limb... 
                                                    //
And abg showing acidosis diagnosed with diabetic keto acidosis 
                                                    //
CT was done  and images showing 
Preseptal cellulitis
                                                     //
KOH mount showing hyphae confirming the diagnosis of Acute rhino oro cerebral mucormycosisi

Anatomical localisation : Medial canthus of left , Oral cavity and hardpalate, left nasal cavity and left frontal & temporal lobes 

etiology: as the patient is diagnosed to have DKA poor control of sugar level in body led to development of mucormycosis.

2a)Inj. Liposomal amphotericin B according to creatinine clearence 
Loading dose 30mg/IV over 2-6 hrs
Maintenance dose 60mg / IV once a day 
&
as the patient is diagnose with DKA  first we need to infuse FLUIDS(3%NS) and monitor electrolye levels and then inj. INSULIN AND MONITOR GLUCOSE LEVEL
   
3A)          Mucormycosis, colloquially known as black fungus, is a serious fungal infection that was seen in far smaller numbers in India before Covid-19, too. But it is now affecting post-Covid patients in large numbers. this surge has been attributed to the improper use of steroids to treat Covid-19 patients, coupled with poorly managed diabetes. But steroids in themselves are not the villains.
“Systemic (oral and intravenous) corticosteroids have been proven to reduce mortality in Covid-19,”
“In addition, India has an epidemic of type 2 diabetes, and a significant proportion of patients with diabetes are diagnosed late in the illness,” which, according to Pinto, could be contributing to this surge in cases.  

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


1A)As the patient has lot of fluid loss  →led to decrease of vol of blood circulating to heart 
decrease of perfusion to lung →development of SOB →after injecting fluids the fluids level in body raised  →decrease of SOB.
2A)2A)  Torsemide is used due to abdominal distension


3A)Treatment for UTI Rationale - used for any bacterial infection .


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

1A)* Patient was apparently asymptomatic 5 yrs back when he had painabdomen & vomitings for which he was taken to a local hospital and treated conservatively.
                                                                            //
Following that he stopped taking alcohol as advised by the physician and was symptom free for nearly 3 yrs.
                                                                            //
Last binge of  alcohol 1 week back following which he again had pain abdomen & vomiting from 1 week and fever from 4 days.
                                                                           //

abdominal pain in umbilical, left hypochondriac, left lumbar and hypogastric regions.

* Abdominal pain was incresed after food intake.

                                                                            //

Pain is throbbing type and radiating to back and is associated with nausea and vomiting( 1 episode) , which is non bilious, non projectile and also has food particles and water content 1 week.

                                                                            //

Fever was high grade, continuous  and associated with chills and rigors.

                                                                            //

Then he developed constipation since 4 days and passing flatus. 

                                                                            //

* patient also had burning micturition since 4 days, which is associated with suprapubic pain, increased frequency and urgency

anatomical localization of pain:abdominal pain in umbilical, left hypochondriac, left lumbar and hypogastric region

alcohol consumption is the primary etiology of patient problem.

2a)TREATMENT ALONG WITH RATIONALE

1) ING. MEROPENAM ; TID for 7 days 

* Meropenem ( broad spectrum Carbepenem ) an antibiotic.

2) ING. METROGYL 500 mg IV TID for 5 days

* inj. Metrogyl has METRONIDAZOLE

Nitroimidazole drug ) an antibiotic

3) ING. AMIKACIN 500 mg IV BD for 5days

* It is an Aminoglycoside antibiotic 

## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.

4) TPN ( Total Parenteral Nutrition )

* Method of feeding that by passes gastrointestinal tract

* Fluids are given to vein , it provides most of the nutrients body needs.

* TPN has proteins, carbohydrates, fats, vitamins, minerals.

5) IV NS / RL at the rate 12l ml per hour

* Given for fluid replacement ie., treat dehydration 

6) ING. OCTREOTIDE 100 mg SC , BD

* It is a Somatostatin long acting analogue.

* It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.

7) ING. PANTOP 40 mg IV , OD

* Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.

8) ING. THIAMINE 100 mg in 100 ml NS  IV , TID

* It is B1 supplement. 

* It is given here because; due to long fasting & TPN  usage , body may develop B1 deficienc

Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.

9) ING. TRAMADOL in 100 ml NS  IV , OD

* It is an opioid analgesic, given to releive pain.

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

1a)
  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 (or when the ventricles relax).
  2. 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.
2a)as the volume of the pericardial fluid is not much raised moreover there is gradual decrease of pericardial fluid compared to the time admission. So, no need of pericardial fluid aspiration

3a)risk factors of patient for acute pericarditis:
DM
HTN
smoking
age
kidney disease

4a) Hb:8g/dl which is low decrease the blood perfusion to organs which finally land in lowBP

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

1A)H/o Surgery for Inguinal hernia 10yrs ago. Patient was fine after the surgery, but had On and Off pain at surgical site which aggravated since 3yrs.
                                                                                    //
H/o Facial puffiness On and Off since 2-3yrs
                                                                                    //
H/o HTN since 1yr.
                                                                                    //
H/o Shortness of breath (Grade II i.e SOB on exertion) 1yr ago for which he visited the local hospital and was diagnosed to be Hypertensive (On medication).

anatomical localization :blood vessels

Etiology: as the patient is hypertensive it affect the vessels increase BP lead to atherosclerotic changes in blood vessels and lead to thrombus formation in coronary vessels.

2a)1. 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.

2. 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

3. 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.



4. 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
5.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

6. Hypoglycemia symptoms explained

7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.

8. 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.

3a)

4a)HYPERTENSION is the main risk 
factors for atherosclerosis in this patient,

5a)A prothrombin time (PT) is a test used to help detect and diagnose a bleeding disorder or excessive clotting disorder; the international normalized ratio (INR) is calculated from a PT result and is used to monitor how well the blood-thinning medication (anticoagulant) warfarin (Coumadin®) is working to prevent blood.


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

1a)
  1. She had H/O heartburn like episodes since a year. They were relived without use of any medication.
  2. She has H/O TB diagnosed 7 months ago for which she completed the course of medication a month ago.
  3. Patient was apparently asymptomatic till 9pm on that day (27/4/21). She apparently ate dinner and slept. When she woke up at night for washroom she developed sweating on exertion and shortness of breath even at rest. 
  4.  came to the OPD with C/O shortness of breath (SOB) since 1/2 hour.
anatomical location: CVS
ETILOGY: Diabetes and hypertension.

2a)
TherapyRecommendations for STEMI
Atorvastatin (Lipitor)40 to 80 mg per day
Morphine4 to 8 mg IV every five to 15 minutes as needed
Nitroglycerin0.4 mg sublingually every five minutes, up to three doses as blood pressure allows
10 mcg per minute IV


3A)


4A)
Complications can include:
  1. Injury to the heart arteries, including tears or rupture
  2. Infection, bleeding, or bruising at the catheter site
  3. Allergic reaction to the dye or contrast used
  4. Kidney damage from the dye or contrast
  5. Blood clots that can lead to stroke or heart attack
  6. Bleeding into the abdomen (retroperitoneal bleeding)


1A)symptamatology; 
*chest pain since 3 days
*profuse sweating and Giddiness since 1 day 
~anatomical localization: BV'S of heart 
~primary etiology; presence of risk factors like HTN AND DM which leads to ATHEROSCLEROSIS

2A)DRUGS GIVEN:

TAB. ASPIRIN 325 mg PO/STAT- COX  inhibitor prevent clot formation

TAB ATORVAS 80mg PO/STAT-atorvastatin reduce LDL and increase HDL

TAB CLOPIBB 300mg PO/STAT-DRUGS GIVENThe 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.

INJ HAI 6U/IV STAT- insulin which help in uptake of glucose using GLUT2 receptor in cardiac tissue, muscle and adipose tissue 

3A)Not necessary
Because patient crossed the window period of 12 hours



                                                                                                                                                                                               

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