27 May
Name - Divya chennamadhavuni , 8th semester
Roll number - 21
1. PULMONOLOGY :
CASE 1: A 55-year-old female with chief complaints of shortness of breath, pedal oedema and facial puffiness.
PROVISIONAL DIAGNOSIS: Acute exacerbation of COPD associated with right heart failure and bronchiectasis.
1A) Her shortness of breath of GRADE 4 is due to the underlying COPD - bronchiectasis ,where there is permanent damage of the large bronchi and bronchioles which makes them abnormally dilated and thickened
Anatomical localization: is in the bronchi and bronchioles
Primary aetiology:
The low oxygen levels due to COPD cause a rise in blood pressure in the arteries of the lungs, a condition known as pulmonary hypertension. This increase in pressure places excess strain on the heart’s right ventricle as it works to pump blood through the lungs. As a result, the heart muscle weakens and right-sided heart failure( cor pulmonale) can occur and can progress to left heart failure too. When too much pressure builds up in the veins and venous return decreases, fluid leaks out into the tissues. Gravity then causes that fluid to move to those parts of the body that are the lowest, that is to the feet and pressure in the main vein connected to the kidneys, may lead to a blockage and a reduced supply of oxygen-rich blood to the kidneys now as the heart starts to fail, renal perfusion fallsrenal failure occurs. The kidneys respond by increasing the production of renin, leading to more aldosterone production, which is consequently followed by sodium and water retention which explains her facial puffiness and ankle oedema. 2A)Mechanisms of the pharmacological interventions:
Head end elevation - relieves the orthopnea in her, as there is orthopnea in a recumbent position
Bipap - it is a type of positive airway pressure ventilator machine that pushes air into the lungs and helps the patient to breathe. It used to maintain a consistent breathing pattern at night or during symptom flare-ups in people with COPD.
The continuous positive air pressure(CPAP) - reduces the cardiac preload by increasing intrathoracic pressure and afterload for patients with heart failure.
Inj lasix( furosemide) - a loop diuretic
Decreases the blood pressure by increasing secretion of Na+ and water
Site of action: inhibition of the sodium-potassium-2 chloride (Na+-K+-2 Cl−) co-transporter (symporter) located in the thick ascending limb of the loop of Henle
Augmentin - amoxicillin + clavulanic acid
Amoxicillin Binds to penicillin-binding proteins on the bacterial cell walls and inhibits the cell wall synthesis
Clavulanic acid inactivates beta-lactamase enzymes in the bacteria.
Azithromycin - A broad-spectrum macrolide antibiotic
With bacteriostatic activity against many Gram-positive and Gram-negative bacteria
Tab.Pantop( pantoprazole) - a proton pump inhibitor
Decreases the amount of acid produced in the stomach, as antibiotics irritate the lining of the stomach and as a response stomach secretes more acid which can cause heartburn in the patient due to reflux of food and acid into the oesophagus
Hydrocortisone (steroid)- anti-inflammatory agent
Neb.with ipravent ,budecortisone -
Ipravent - anticholinergic bronchodilator - relieves breathlessness
Budesonide( steroid) - potent anti-inflammatory agent
Tab. pulmoclear - mucolytic agent
It loosens the mucus so that it comes out easily while coughing
Inj .thiamine - a water-soluble vitamin
Intravenous thiamine supplementation had some positive effect on oedema and systolic function through an increase of lateral and septal Sm.
Thiamine, in critically ill patients, is sought to increase oxygen utilization (vo2)
Chest physiotherapy -
The purpose of chest physiotherapy is:
- To facilitate the removal of retained or profuse airway secretions.
- To optimize lung compliance and prevent it from collapsing.
- To decrease the work of breathing.
Vitals monitoring - this is of prime importance as vitals predict the events of the condition going in a normal or an abnormal way.
I/O charting - One of the primary problems with heart failure is excess fluid in the body, which
the heart must pump to the kidneys to excrete.To avoid this fluid overload, patients need to monitor their daily fluid intake.
3A) The acute exacerbation in this patient can because of any secondary infections in the lungs, upper respiratory tract etc.
pollens triggered allergies can also cause exacerbation of COPD and she even has a history of working in the paddy fields!
4A) ATT might not have affected her symptoms?
rifampicin can cause renal failure which is very rare, could be a reason for her facial puffiness too.
5A) hyponatremia seen can be because of more water retention compared to sodium retention?
She has respiratory acidosis( due to hypercapnia) with compensated metabolic alkalosis which can be a reason for her hypochloremia.
NEUROLOGY :
CASE - 2: A 40 year old male presented to the OPD with the chief complaints of irrelevant talking and decreased food intake since 9 days.
Ans1) Symptomatology in terms of event timeline :
on 15 may - got admitted
9 days back - started talking and laughing to himself
decreased food intake
short-term memory loss
4 months ago - had seizures (on stopping alcohol consumption)
1 year ago - had seizures
2 years ago - diagnosed with diabetes
Primary aetiology :
Alcohol withdrawal and GABA : mechanism -
Ethanol is a CNS depressant
Normally, during acute intoxication of alcohol,
Dopamine is responsible for the euphoric effects as it is released from the reward centers in the brain.
There is increase of GABA effects especially in receptors with delta subnits ,so the responses in the brain are slowed .The delta subunits of GABA receptors are mainly distributed on brainstem, cerebellum, thalamic replay cells , hippocampus which explains the intoxication symptoms of alcohol
Abrupt withdrawal is thought to reduce inhibitory neurotransmission and enhance excitatory neurotransmission.
constant consumption of alcohol down regulates the GABA receptors in order to maintain homeostasis and there is counter-regulation of excitatory neurotransmitters like NMDA , GLUTAMATE -think of it like a see-saw trying to balance
When alcohol is no longer consumed -down-regulated GABA receptor complexes are so insensitive to GABA that the typical amount of GABA produced has little effect and abrupt withdrawal of alcohol leads to glutamate-mediated excitation leading to autonomic overactivity and neuropsychiatric problems - delirium and seizures. Dopamine levels are increased which contributes to autonomic hyperarousal and hallucinations
Compounded with the fact that GABA normally inhibits action potential formation (now there are not as many receptors for GABA - tachyphylaxis), sympathetic action will be unopposed now
ie; tachycardia, tremors etc
Ans2) Mechanisms of pharmacological interventions:
1.IVF NS and RL - to combact the dehydration in him as alcohol dries out the body as it reduces ADH and decreases urine formation and this exacerbates the diuretic effect and leads to dehydration.
2.Inj.Thiamine - thiamine deficiency is common in chronic alcoholics and can be a cause to develop wernicke encephalopathy in him
3.Inj.lorazepam - a benzodiazepine
Has GABA inhibitory actions and also
Provides a long duration of seizure
Control
4.Tab. Pregabalin - anti-epileptic drug
5.Inj. HAI SC - human rapid
A short-acting insulin
6.Lactulose - an Osmotic laxative
For of hepatic encephalopathy if present? As lactulose decreases the ammonia from the blood by drawing it into the colon and excreting it.
7.Syp.potchlor -for potassium suppliementation.
Ans3) Couldn't find a proper answer
Ans4) To prevent Wernicke's encephalopathy or if it has already occurred - to treat it.
Ans5)
Ans6)Alcohol is said to decrease the precursor cells in the bone marrow resulting n fewer mature red blood cells being madealcohol also impact the maturation of red blood cells, causing abnormality (shapes) or dysfunction of the cells. When enlarged red blood cells (due to alcohol) are produced, as a complication, they are likely to be destroyed faster than normal cells. Anaemia can be a complication of renal failure too.
Ans7) chronic alcoholism can cause vitamin deficiencies
So our patient also might have landed upon VITAMIN -B12 deficiency
He is a diabetic who is not good at keeping it in good control by taking his medicines regularly
Type 2 DM and VITAMIN B12 deficiency has 3 times higher risk of developing diabetic foot ulcers than those with normal B12 levels
SO could this be a co-relation to his ulcer?
CASE 3 - A 52-year-old male with cerebellar ataxia
Ans1) Symptomatology evolution -
7 days back - giddiness, one episode of vomiting
Asymptomatic for 3 days
Took alcohol and then developed
- giddiness of sudden onset, bilateral hearing loss, aural fullness, tinnitus
Vomitings 2-3 episodes per day (non-projectile, non-bilious, containing food particles)
Postural instability
2 days back - slurring of speech and deviation of the mouth
Anatomical localization: it is a cerebellar infarct which is can be because of an ischemic stroke
So the location is in cerebellar blood vessels mostly in the arteries.
Primary etiology : stroke can be arterial (99%) and venous (1%) in origin
strokes are divided into ischemic (85%) and hemorrhagic(15%) .
ischemic can be because of thrombotic (25%) or embolic (60%)
- Ischemic strokes are caused by arterial obstructions that impair blood and oxygen delivery directly .This can be either through migration from the heart or directly at the vessels
Thrombotic strokes can travel from large to small vessels and these can be due to atherosclerosis (most common) or other vasculopathy, including arterial dissections, typically of the vertebral arteries in cerebellar strokes , vasculitis, hypercoagulable states
Embolic strokes - artery to artery embolic stroke ( carotid atherosclerosis ) is more common followed by cardiac embolic strokes as in atrial fibrillations (most common)
- Hemorrhagic strokes are usually caused by arterial bleeding that directly damages brain tissue or obstructs vascular flow through elevated local pressure.
The patient is hypertensive and high blood pressure is an important risk factor for stroke.
Blood vessels damaged by high blood pressure can narrow, rupture or leak. High blood pressure can also cause blood clots to form in the arteries, blocking the blood flow and potentially causing a stroke.
He had his symptoms aggravated on taking alcohol which can be because,
drinking too much alcohol raised his blood pressure?
hypertension might have induced atherosclerosis in him and this lead to the stroke in him?
a
Ans2) Pharmacological interventions :
1. Tab. Vertin - a betahistine
To combat vertigo, giddiness and tinnitus in him
As it improves the blood flow to the inner ear which reduces the pressure in the inner ear fluids.
2. Inj.Zofer - Ondansetron ( selective 5-HT3 receptor antagonist)
Inhibits serotonin and decreases nausea and vomitings in the patient.
3. Tab. Ecosprin - an antiplatelet drug
So inhibits clot formation in his blood vessels
4. Tab.Atorvostatin - a HMG -CoA reductase enzyme inhibitor
Decreases the cholesterol levels in him ans high cholesterol is a risk factor for stroke.
5. Tab.Clopidogrel - an inhibitor of platelet activation and aggregation and prevents them from forming harmfull clots.
6. Inj. Thiamine - fatigue related to stroke could benefit from thiamine?
Ans3) I think he's being, hypertensive is the cause of his cerebrovascular accident?
Ans4) As mentioned in the primary aetiology of stroke in this patient, alcohol would have elevated his blood pressure leading to aggravation of his symptoms?
CASE 4: A 45-year-old female with palpitations, pedal oedema, chest heaviness, radiating pain along the left upper limb.
Ans1) Anatomical localization - cervical vertebrae - cervical spondylosis
Primary aetiology - Hypokalemia:
Which causing the symptoms - palpitations, chest heaviness, shortness of breath, swelling over legs in her -Potassium levels below 3,0 mmol/l cause significant Q-T interval prolongation with subsequent risk of arrhythmias (torsade des pointes, ventricular fibrillation and) sudden cardiac death.
Arrthymias can lead to heart failure which explains her pedal edema, chest pain, shortness of breath?
in this patient hyopkalemia could be because of the loop diuretics used
Or
Can it be a bartter syndrome or a Gitelmansyndrome?
But her magnesium levels are not known and neither her calcium excretion decreased nor increased.
Ans2) The recurrent hypokalemia is may be due to loop diuretics in this patient?
Risk factors of hypokalemia :
Heart failure, CKD,DKA
Hypertension
Alcoholism
Cushing's syndrome
Primary aldosteronism
Abnormal losses :
Medications- Diuretics, Beta sympathomimetics
Laxatives
Steroids
Amphotericin B
Insulin overdose
Aminoglycosides
Decongestants
Gastrointestinal losses
Renal losses - osmotic diuresis
Mineralocorticoid excess
Hypomagnesemia
Intrinsic renal transport defects
Transcellular defects- Alkalosis
Thyrotoxicosis
Hypothermia
Inadequate intake
Pseudo hypokalemia
Ans3) ECG changes in hypokalemia
_ QT prolongation also can be seen
CASE 5 - A 55-year-old male with seizures
Ans1) Stroke causes brain injury and results in the formation of scar tissue, which affects the electrical activity in your brain and disrupting the electrical activity can cause us to have a seizure.
There are several causes for early-onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury (particularly after carotid endarterectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after haemorrhagic strokes are thought to be attributable to irritation caused by-products of blood metabolism. The exact pathophysiology is unclear, but an associated ischaemic area secondary to haemorrhage is thought to play a part. Late-onset seizures are associated with persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Haemosiderin deposits are thought to cause irritability after a haemorrhagic stroke.
Ans2) Early-onset seizures in him might have presented with a focal onset - partial seizures - (as he was conscious during the seizure activity)
while tonic‐clonic seizures that were generalised - (as he was unconscious during the seizure activity )which occurred later might be because of late-onset seizures in him.
CASE 6- A 48 year old male with seizures and altered sensorium
Ans1) The ataxia in him can be either due the impaired coordination due to the damage of brain tissue in stroke or may be due to his alcohol abuse too.
Ans2) Chronic alcoholism can cause alcoholic thrombocytopenia and alcohol also rises the blood pressure due to which vessels can rupture .These factors might have contributed to his IC bleed? Though rare, severe thrombocytopenia can cause bleeding into the brain which can be fatal.
CASE 7 - 30 year old male patient with weakness of right upper limb , lower limb and deviation of mouth to left
Ans1) YES. He might have injured his head during the accident and got a concussion on his brain and due to the trauma ,his blood vessels in the brain and neck might have got tears and cuts which lead to hemorrhage, formation of clots in his vessels and obstructed them causing ischemic penumbra's at the sites of hypo perfusions .
Ans2) Warning signs of stroke :
Ans3) Pharmacological interventions:
1.Inj.Mannitol - osmotic diuretic
Usefull in relieving the edema in the process of brain tissue damage?
2.Tab. Ecosporin - antiplatelet drug
3.Tab. Atorvastatin - a HMG CoA reductase inhibitor so it inhibits cholesterol synthesis and prevents the incidence of stroke as hypercholesterolemia is a risk factor for stroke
Ans4) As he drinks moderately I don't think alcohol might have played any significant role in his CVA.
Ans5) Studies have demonstrated a trend toward a higher risk of stroke with lower HDL-C and support HDL-C as an important modifiable stroke risk factor.
In patients with recent stroke or transient ischemic attack and no coronary heart disease, only lower baseline HDL-C predicted the risk of recurrent stroke.
CASE 8 - A 50-year-old male with cervical myelopathy
Ans1) Myelopathic hand -
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"
Ans2) finger escape sign - when patient holds fingers extended and adducted, the small finger spontaneously abducts due to weakness of intrinsic muscle.
Ans3)Hoffmann's sign - snapping patients distal phalanx of middle finger leads to spontaneous flexion of other fingers
CASE 9-A 17 year old female with seizures
Ans1) Her cause could be cortical vein thrombosis.
Ans2)Risk factors for children and infants include:
- Problems with the way their blood forms clots
- Sickle cell anemia
- Chronic hemolytic anemia
- Beta-thalassemia major
- Heart disease — either congenital (you're born with it) or acquired (you develop it)
- Iron deficiency
- Certain infections
- Dehydration
- Head injury
- For newborns, a mother who had certain infections or a history of infertility
Risk factors for adults include:
- 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
Ans3). she was administered antiepileptic drugs which have seizure free periods as the drug effects wanes off the seizures appear again or when we withdraww them seizures appear againaccording to some studies, antiepileptics can be withdrawn only after a sufficient seizure free period of 2 years.
Ans4) Anticoagulants - HEPARIN
CARDIOLOGY :
CASE 10 - A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS
Ans1) Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure.
Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure.
Ans2) Pericardiocentesis is not done here may be because the effusion was resolving itself? resolving : 2.07cms effusion at the time of admission -1.4mm at the time of discharge.
Ans3) The risk factors for heart failure in him are: Hypertension, Diabetes ,Smoking , Alcoholism.
and his age too.
Ans4) maybe because of the pressure exerted by the extra fluid around the heart, it is unable to pump the blood to its optimum which is contributing to hypotension?
Ans1) Reason for his heart failure can be:
1.Diabetes -Diabetic patients have an increased risk of developing heart failure because of the abnormal cardiac handling of glucose and free fatty acids (FFAs), and because of the effect of the metabolic derangements of diabetes on the cardiovascular system. High blood sugar can damage blood vessels and the nerves that control your heart.
2.He is a hypertensive
As per his 2D-Echo is he having diastolic dysfunction LVH, MR and TR with PAH
He can be having Heart failure with preserved ejection fraction.
Ans2) Anaemia can be because of decreased erythropoietin production of kidneys due to diabetic nephropathy he is having.
Ans3)Diabetic bullae, also known as bullosis diabeticorum, is a spontaneous, distinct, non-inflammatory, blistering condition of the skin predominantly seen in patients with diabetes mellitus
Circulation of blood at wound site is critical for healing of the wound .In diabetes due to narrow blood vessels less oxygen reach the tissues and wounds do not heal quickly.
Ans4) He showed DIABETIC TRIOPATHY
_ Diabetic neuropathy followed by retinopathy and nephropathy.
CASE 12 -A 52yr old male came to the OPD with the chief complaints of decreased urine output and shortness of breath at rest since one day.
Ans1) Evolution of the symptomatology -
- H/o Facial puffiness On and Off since 2-3yrs.
- 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).
- H/o HTN since 1yr.
- Patient was apparently asymptomatic 2 days ago when he developed Shortness of breath Grade II (on exertion) which progressed to Grade IV (at rest) for which he visited local RMP and was referred to our hospital.
- Patient also complains of decreased urine output since 2 days and Anuria since morning.
anatomical location - Blood vessels , heart chambers
Primary etiology - could be due to the ASD which might have lead to AF in him ,as a result the heart beats and contracts irregularly, blood flow may slow or pool and cause the formation of clots due to stasis of blood in the atrial chambers
hypertension could have also predisposed to the formation of thrombi - by causing endothelial dysfunction
which leads to atherosclerosis which can also be a cause of thrombus formation in him
THE AF might have progressed to heart failure due lo low cardiac output which explains his orthopnea ,as a result renal perfusion decreased( renal failure) and lead to activation of renin causes - sodium water retention by Aldosterone actions -volume overload which explains his facial puffiness and vaso constriction which aggravates hypertension again.
Ans2) pharmacological interventions-
1. TAB. Dytor - spironolactone acts by antagonizing the effect of aldosterone,
2. TAB. Acitrom - anticoagulant
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 - Carvedilol an alpha and beta blocker it helps in decreasing heart rate, blood pressure, and load on the heart.
4. INJ. HAI S/c -( human atrapid )-short acting insulin
5.TAB. Digoxin - 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 monitered as he is on anticoagulants
Ans3) Cardio renal syndrome seen in this patient is either type 2 or 4
mechanism explained in the primary etiology part.
Ans4) Hypertension?
Ans5) may be because he is on anticoagulant.
CASE 13 - 67 year old patient with acute coronary syndrome
Ans1) Evolution of the symptomatology -
DM2 since 12 years and is on Rx GLIMI M2 PO/BD
She had H/O heartburn like episodes since a year. They were relived without use of any medication.
She has H/O TB diagnosed 7 months ago for which she completed the course of medication a month ago.
H/O pulmonary TB 7 months ago when she had cough, chest pain. Completed the course for TB a month ago. Currently negative for TB.
Hypertension since 6 months and is on Rx TELMA 20 mg PO/OD
C/O shortness of breath (SOB) since 1/2 hour
Anatomical localization - Blood vessels
Primary etiology -ACS is the clinical syndrome of an acute occlusion within an already diseased coronary artery.
Aetiologically, coronary artery disease is closely tied to HTN, diabetes mellitus (DM), dyslipidemia, metabolic syndrome and obesity among other factors
The combination of poor diabetes control and uncontrolled HTN is responsible for a great percentage of the incidence of ACS
Ans2) Pharmacological interventions -
1.TAB MET XL 25 MG/STAT - anti-hypertensive medicine used to treat high blood pressure and various other heart-related conditions such as angina (chest pain), heart failure. It contains metoprolol( beta blocker) as an active ingredient having action specific to the heart muscles.
2.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
In this case a PCI was not done due to non availability of vacancies in higher centres due to the ongoing pandemic. Instead she was sent home with a prescription.
Ans3).Percutaneous Coronary Intervention -
CASE 14- CASE DISCUSSION ON ACUTE MYOCARDIAL INFARCTION.
Ans1) Evolution of the symptomatology -
The patient is a known case of hypertension and type 2 diabetes.
3 days back and then he developed mild chest pain in the right side of the chest. The pain was insidious in onset and gradually progressive. The pain was of dragging type and was radiating to the back (retrosternal pain).
Anatomical location - blood vessels
primary etiology - Atherosclerosis – Also known as coronary artery disease, this condition is the most common cause of heart attacks and occurs when the buildup of fat, cholesterol, and other substances forms plaque on the walls of the coronary arteries can be the cause of his myocardial infraction
RISK FACTORS HE IS HAVING ARE - diabetes and hypertension
Ans2) pharmacological interventions -
1.TAB. ASPIRIN -
: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.
2.Tab. atorvas -Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. statin medications decrease cholesterol production in the liver.
3.TAB CLOPIBB - an inhibitor of platelet activation and aggregation and prevents them from forming harmfull clots.
4.INJ HAI - human actrapid - short acting insulin.
5.ANGIOPLASTY
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.
Ans3) I think the second PTCA was unnecessery.
GASTROLOGY
CASE 15 -A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA
ANS1) Antomical location - pancreas
primary etiology -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 secretory transport and by an activation of pancreatic enzymes Attributed to alcohol.
Ans2) Pharmacological interventions -1) ING. MEROPENAM - used to prevent septic complications as it is a bacteriostatic agent.
2) ING. METROGYL -Metronidazole used against various anaerobic organisms.
3) ING. AMIKACIN - an aminoglycoside.
4) TPN ( Total Parenteral Nutrition )- the early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infection; TPN is only required in a few patients.
5) IV NS / RL - to combat fluid loss in pancreatisits
6) ING. OCTREOTIDE - cause insulin suppression.
7) ING. PANTOP - inhibits the proton pump and decreases acid secretion.
8) ING. THIAMINE- 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.
9) ING. TRAMADOL - centrally acting analgesic.
CASE 16 - CASE DISCUSSION ON 25 YEAR OLD MALE WITH EPIGASTRIC PAIN
Ans1) pleural effusion?
Ans2) may be due to decreased insulin, secretion from the damaged pancreatic beta cells.
Ans3) Because of the ongoing hepatic cell injury?
Ans4) 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
CASE 17 - A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension
Ans1) Ruptured liver abcesses can spread to the heart ,lungs ,brain ,eyes .she also might have landed on hemoperitoneum
Ans2) may be due to the blood loss leading to shock and the infection spreading in the blood and causing sepsis?
Ans3) may be due to NSAID usage as they are known to be hepatotoxic.
CASE 18 - post TURP with non-oliguric ATN
Ans1) Metabolic acidosis?
Ans2) Intracellular acidosis might be the cause.
Ans3) papillary necrosis due to hydronephrosis.
TURP is causing hydronephrosis due bladder obstruction and causing urinary back flow into the kidneys leads to papillary necrosis
CASE 19 -An Eight year old with Frequent Urination
The primary features of ADHD include inattention and hyperactive( restlessness)-impulsive behavior. ADHD symptoms start before age 12, and in some children, they're noticeable as early as 3 years of age ADHD symptoms can be mild, moderate or severe, and they may continue into adulthood.
ADHD occurs more often in males than in females, and behaviors can be different in boys and girls. For example, boys may be more hyperactive and girls may tend to be quietly inattentive
pathophysiology -
ADHD presents with low dopaminergic functioning. Typically, a number of genes are involved, many of which directly affect dopamine neurotransmission.
In children with ADHD, there is a general reduction of volume in certain brain structures, with a proportionally greater decrease in the volume in the left-sided prefrontal cortex The posterior parietal cortex also shows thinning in individuals with ADHD compared to controls. Other brain structures in the prefrontal-striatal-cerebellar and prefrontal-striatal-thalamic circuits have also been found to differ between people with and without ADHD
The subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with control .Inter-hemispheric asymmetries in white matter tracts have also been noted in children with ADHD, suggesting that disruptions in temporal integration may be related to the behavioral characteristics of ADHD
studies have shown children with ADHD have significantly higher rates of incontinence, constipation, urgency, infrequent voiding, nocturnal enuresis and dysuria than those without ADHD.
Ans2) his routine urine examination reports are normal.
Although the cell counts in the urine examination, and there are no microorganisms after urine culture , still due to the presence of some mildly enlarged mesenteric lymph nodes, there still remains suspicion of an infective etiology, including cox bacilli
.From the history of excessive hyperactivity , impulsiveness , lacking of attentivity , a though goes towards Attention Deficit Hyperactivity Disorder (ADHD) and in turn towards the association urination disorders. ADHD is not a neurogenic but a psychomotor disorder so this might be the cause of him not having any urinary urgency at night during his sleep
Ans3) behavioral therapies in ADHD are the recommended first line treatment in those who have mild symptoms or are preschool-aged
Psychological therapies used include: psycho educational input, behavior therapy, cognitive behavioral therapy inter personal psychotherapy, family therapy, school-based interventions, social skills training, behavioral peer intervention, organization training and parent management training, Neuro feedback has been used but it is unclear whether it is useful Parent training may improve a number of behavioral problems including oppositional and non compliant behaviors
Stimulant medications are the pharmaceutical treatment of choice .They improve symptoms in 80% of people, although improvement is not sustained if medication is ceased.
the treatment for his frequent urination could be planning a proper toileting schedule to make his body acclametize to normal voiding pattern and some pelvic floor excercises would surely help alomg with the management of is hidden anxiety and stress too.
CASE 20 -A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH
Ans1) Physical findings of a TEF
Abdominal distention may occur in TEF secondary to collection of air in the stomach
Symptoms of a TEF
Common presenting symptoms include recurrent pneumonias, hemoptysis, and coughing episodes following eating.
Ans2) Immune reconstitution inflammatory syndrome (IRIS) is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.
AS our patient is in an immuno compromised state for being RVD positive she will be prone opportunistic many infections and reinfections too So she is susceptable to IRIS, she should be started on ATT and ART.
INFECTIOUS DISEASE ANG HEPATOLOGY
CASE 21 -LIVER ABCESS
Ans1) YES. locally made alcohol is the main cause of his liver abcess because it can be completely unhygienic with lots of harmful micro organism causing various diseases in humans
Ans2)Mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver.
Ans3) yes ,liver abcess are more common on right lobe because ,
Ans4) indications for ultrasound guided aspiration of liver abscess
- pain and impending rupture
-Not responding to medical treatment
-secondary infections causing septicemia
-Any life threatening hemorrhage
CASE 22- A case discussion on liver abcess of a 21- year-old male
Ans1) Toddy is a local alcoholic beverage which again can be very unhygienic and lead to liver abcess.
Ans2) Approach of a patient with amoebic liver abcess
Ans4) we treat both the amoebic and pyogenic liver abcess here may be because we are not 100%sure if it is amoebic liver abcess only-if we don't take proper percautions secondary bacterial infections can occur
Ans5) specific tests diagnostic for entameba histolytica
USG abdomen
CT ,chest radiographs
CASE 23- 50/Male came with altered sensorium
Ans1) Evolution of symptomatology-
Hypertensive since 3 years.
He went for covid 19 vaccination and had fever with chills and rigor.
Facial puffiness and periorbital edema after 10 days of vaccination
He developed weakness in right upper and lower limb.
A week later , he presented with altered sensorium
Anatomical localization - maxillary sinus
primary etiology - he got ACUTE ORO RHINO ORBITAL MUCORMYCOSIS due to poorly controlled diabetes
Ans2) pharmacological interventions -
Inj. Liposomal amphotericin B
200mg of itraconazole
these are antifungal drugs preferably given to mucormycosis patients
Ans3) Reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time
-high usage of steroids as a treatment for COVID-19 might have help us in coping up with the virus but have made the patients immunosuppressive which make them succepteble to various infections and increased blood sugar levels or poorly controlled blood sugar levels added up the with reason for rise in the incident of black fungs!
INFECTIOUS DISEASE (COVID-19)
Covid master chart
MEDICAL EDUCATION
Monthly assignmemt,
It has been an amazing experience going through all the cases in detail and understanding the concepts in depth with clinical knowledge added which makes them even more interesting.I feel good that i got to learn few physiology concepts relating all the organ system with each other in a generalised way and applying them on the patients condition in order to understand the etiologies and answer the questions .
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