JUNE BIMONTHLY ASSESSMENT
PULMONOLOGY
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html
1) What is the evolution of the symptomatology in this patient interms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient's problem?
Ans :- Evolution of symptomatology
• 1st episode of sob - 20 yrs back
• 2nd episode of sob - 12 yrs back
Then onwards, she has been having yearly episodes of sob for the past 12 yrs.
》Diagnosed with diabetes - 8yrs back
》Anemia and took iron injections - 5yr ago
》Generalised weakness - 1 month back
》Diagnosed with hypertension(HTN) - 20 days back
》Pedal edema - 15 days back
》Facial puffiness- 15 yrs back
~ Anatomical location of problem - Lungs
~ Primary etiology of patient- usage of chulha for prolonged period (20 yrs)
2) What are the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patient?
Ans :- Head end elevation : MOA;
• Improves oxygenation
• Decreases the incidence of VAP
• Increases hemodynamic performance
• Increases end expiratory lung volume
• Decreases incidence of aspiration
》Indication: head injury
meningitis
pneumonia
•oxygen inhalation to maintain spo2
•Bipap : Non invasive method (bipap is bilevel positive airway pressure)
》MOA : Assist ventilation by delivering positive expiratory and inspiratory pressure with out the need for ET incubation.
3) Cause for current acute excerbation
Ans :- It could be any infection.
4) Could the ATT affected her symptoms if so how?
Ans : Yes! ATT (Anti tubercular treatment) affected her symptoms.
Isoniazid and rifampicin are nephrotoxic drugs. Urea and creatinine levels( RFT) are elevated.
NEUROLOGY
CASE A
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
1) What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans: Evolution of symptomatology
Irrelevant talking and laughing - since 9 days
Decreased food intake - since 9 days
short term memory loss - since 9 days
The above symptoms may occur due thiamine deficiency...Thiamine deficiency occurs either due to..
1) Decreased absorption from intestine ( Hereditary condition)
2) Inadequate nutrition etc..
He had developed seizures following stoppage of alcohol intake for 24hours which is due to this reason:- Alcohol affects the way in which nerve cells communicate. receptors are some specialized proteins on the surface of nerve cells which receive chemical signals from one another. Due to long-term alcohol intake, receptors affected by alcohol undergo adaptive changes to maintain normal function.
The two important brain communication systems affected by alcohol involve the neurotransmitters: gamma-aminobutyric acid and glutamate.
The GABA system:
GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling. single doses of alcohol facilitate the inhibitory function of the GABA receptor, contributing to alcohol intoxicating effects. During withdrawal, brain GABA levels fall below normal and GABA activity declines. The combination of reduced brain GABA levels and GABAa receptor sensitivity may be contributed an adaptation to the presence of alcohol. In the absence of alcohol, the resulting decrease in inhibitory function may contribute to Symptoms of nervous system hyperactivity associated with both acute and protracted AW.
The glutamate system:
The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures. Alcohol inhibits the excitatory function of the NMDA receptor in laboratory studies at concentrations associated with mild to moderate alcohol intoxication in humans. As with the increased inhibitory function of the GABAA receptor, the decreased excitatory function of the NMDA receptor is consistent with alcohol’s general sedative effect. Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function. Persistent alterations in NMDA receptor function may potentiate the neurotoxic and seizure-inducing effects of increased glutamate release during withdrawal.
THE PATHOPHYSIOLOGY:
Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.
The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease. The increase in levels of urea, creatinine, uric acid leads to uraemic encephalopathy. which causes asterixis.
The deficiency of thiamine and increase in levels of toxins in the body due to renal disease is the primary etiology of the patient's problem.
2) What are the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
Ans: I) Thiamine helps the body cells change carbohydrates into energy. It has been used as a supplement to cope with thiamine deficiency
ii)Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.it enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
iii)pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.
iv)Lactulose is used in preventing and treating clinical portal-systemic encephalopathy .its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia.
v)Potchlor liquid is used to treat low levels of potassium in the body.
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier ? what could be a possible cause for this time?
Ans : Excess thiamine deficiency and excess toxins accumulation which occcured due to renal disease caused by excess alcohol addiction.
4) What is the reason for giving thiamine in this patient?
Ans : Chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine,Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine, and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death.
5) What is the probable cause for kidney injury in this patient?
Ans: The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease.
6) What is the probable cause for the normocytic anaemia?
Ans : Alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron .alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption from intestine .
7) Could chronic alcoholism have aggravated the foot ulcer formation ?if yes and why ?
Ans : yes,As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic theimmune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.
CARDIOLOGY
CASE - A
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html
1)What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans:- Heart failure with preserved ejection fraction occurs in conditions where there is diastolic dysfunction of the ventricles like hypertrophic cardiomyopathy and restrictive cardiomyopathy. The ventricles are unable to relax completely , but they contract adequately , there by maintaining the ejection fraction.
Heart failure with reduced ejection fraction occurs in intrinsic heart diseases like DILATED CARDIOMYOPATHY. The ventricles are dilated and their wall is thinned out in this condition. There will be systolic dysfunction of the ventricles leading to reduced ejection fraction.
2)Why haven't we done pericardiocentesis in this patient?
Ans:- Pericardiocentesis is indicated when there is considerable pericardial effusion causing compression over the heart chambers. In this condition, there is no need for pericardiocentesis as it is resolving.
3)What are the risk factors for development of heart failure in the patient?
Ans:- Hypertension, CAD, DM, MEDICATIONs.
4)What could be the cause for hypotension in this patient?
Ans:- Systemic venous return to the heart is reduced which in turn reduces the pulmonary venous return. This causes decrease in the end diastolic volume and finally reduced cardiac output.
CASE - A
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans:- COURSE OF THE SYMPTOMS-
• Pain abdomen and vomiting was treated conservatively 5yrs ago.
• Pain abdomen and vomiting for 1 week.
• Constipation, burning micturition, fever for 4 days.
After admission:-
• CT scan - showed Pseudocyst.
• Chest X ray - showed left pneumothorax and left pleural.
》ANATOMICAL LOCATION: Pancreas
》Primary etiology: Chronic alcohol intake
2) What is the efficacy of drugs used along with other non-pharmacological treatment modalities and how would you approach this patient as a treating physician?
Ans:- Placebo has no physiological and pharmacological actions.
• DRUG THERAPY:-
Amikacin, Metronidazole and Meropenem are all given to control infection.
TPN (Total Parenteral Nutrition) - It is given to bed ridden patients.it contains carbohydrates, proteins, fats vitamins and minerals.
NS/RL - It is given as fluid replacement in order to combat dehydration.
Tab. Pantop - It is a proton pump inhibitor. It is used in this case for its anti-pancreatic secretory.
• Inj. Octreotide –
It is a somatostatin analogue.
It decreases the secretions of pancreas.
It also has anti-inflammatory and cytoprotective effects.
• Inj. Thiamine -
It is B1 supplement.
It is given here because; due to long fasting & TPN usage, body may develop B1 deficiency.
Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplementation is necessary.
• Inj. TRAMADOL -
It is an opioid analgesic which is given to relieve pain.
CASE - A
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
1. What could be the reason for his SOB?
Ans:- Reason for his sob can be POST TURP SYNDROME: it occurs because of irrigation of absorption of large volumes of irrigation fluid during TURP which can cause HYPONATREMIA, CARDIORESPIRATORY depression.
2. Why does he have intermittent episodes of drowsiness?
Ans:- Drowsiness indicates that the brain tissue is not getting enough oxygen supply. This could be due to anemia. Another possibility is due to electrolyte imbalance in the patient.
3. Why did he complaint of fleshy mass like passage in his urine?
Ans:- Patient has UTI (pyuria). This was felt like a fleshy white mass by the patient.
4. What are the complications of TURP that he may have had?
Ans:- COMPLICATIONS OF TURP:
~Bladder perforation
~Coagulopathies
~Bleeding
~Transient bacteremia and septicemia.
~Toxicity due to irrigating fluids.
~Hypothermia.
INFECTIOUS DISEASES ( HI VIRUS, MYCOBACTERIA)
CASE - A
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
1)Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
Ans:- Clinical history and physical findings:
> Cough since 2 months on taking food and liquids
> Difficulty in swallowing since 2 month
> H/O weight loss of 10 Kgs since 2 months, hoarseness of voice
> Incapable of food intake
> Oro pharyngeal regurgitation
2)What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Ans:- A retrospective analysis examining all forms of IRIS, 33/132 (25%) of patients exhibited one or more disease episodes after initiation of ART. Other cohort analyses examining all manifestations of IRIS estimate that 17–23% of patients initiating ART will develop the syndrome.
INTERVENTION: The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression.
INFECTIOUS DISEASES AND HEPATOLOGY
CASE - A
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
1)Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it? What could be the cause in this patient?
Ans:- yes, it could be due to intake of contaminated toddy.
2)What is the etiopathogenesis of liver abscess in a chronic alcoholic patient? (since 30 years - 1 bottle per day)
Ans:- According to some studies, alcoholism 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.
3)Is liver abscess more common in right lobe?
Ans:- Yes right lobe is involved due to its more blood supply
4)What are the indications for ultrasound guided aspiration of liver abscess?
Ans:- Indications for USG guided aspiration of liver abscess:
▪︎ Amoebic liver abscess
▪︎ Large abscess more than 6 cms.
▪︎ Left lobe abscess
▪︎ Caudate lobe abscess
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