MEDICINE CASE BASED LEARNING || Online assignment for the month of MAY 2021
MEDICINE BLENDED ASSIGNMENT
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
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.
- 1st episode of SOB 20 years ago was of Grade 2. Lasted one week. Relieved on medication
- Next 8 years, similar events every January which lasted 1 week, grade 2 severity. Relieved on medication
- Was diagnosed with Diabetes 18 years ago
- 2nd severe episode of SOB 12 years ago and was of grade 2 type. Lasted 20 days. Relieved on hospitalization and treatment
- Next 12 years, each SOB incident started every January and lasted 30 days
- Latest episode started one month ago in April, is persistent since 30 days with grade 3 dyspnea.
- 20 days ago, She was diagnosed with Hypertension
- 15 days ago she started developing pedal edema and facial puffiness
- Since 2 days ago, severity of breathlessness went up to grade 4 dyspnea (SOB at rest) not relieved on Nebulization along with decreased urine output and drowsiness.
- Anatomical localization:
- Right paracardiac localization of COPD
- The possible etiological factors could be the following:
- Exposure to allergens which could make it a possible occupational hazard
- Infections by Moraxella, H. influenzae or Pneumococcus
- Dust or pesticides exposure.
Furosemide :
- MOA: Blocking Na-K-Cl co transporter in loop of Henle > loss of K, Na and Cl in urine
- Indication: 2D Echo was suggestive of potential development of Right Heart failure
- Efficacy: Furosemide is the Ideal for the loop diuretic therapy in Heart failure
- Reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038646
Budisonide
- MOA: Inhibit inflammatory cytokine production
- Indication: The dyspnea that was suggestive of COPD
- Efficacy : Budesonide/formoterol reduced the mean…
- Exposure to allergens which could make it a possible occupational hazard
- Infections by Moraxella, H. influenzae or Pneumococcus (Bacterial), Influenza, Rhinovirus, Coronavirus (Viral)
- Dust or pesticides exposure
- An episode of seizure (GTCS) one year ago
- Latest episode of Seizure 4 months ago associated with restlessness, sweating, and tremors following cessation of alcohol
- 9 days ago, patient developed Altered mental state with discontinuous spatial and temporal orientation, loss of appetite, weakness
- After admission, tremors, sleep disturbances, sweating
- Involuntary rolling of eyes, tongue biting, frothing, loss of consciousness
- Uremic encephalopathy is usually confined to basal ganglia, thalamus and midbrain
- Wernicke’s encephalopathy is normally localised to frontal lobe, thalamus and hypothalamus.
- Alcohol use disorder in addition to poor appetite leading to Vit. B1 (Thiamine) deficiency
- Uremia could be secondary to prerenal acute kidney injury
- MOA: Replenishment of the thiamine lost reserves of Thiamine
- Indication: Chronic Alcoholism could be a potential cause of Thiamine deficiency
- Efficacy: For the treatment of acute Wernicke’s encephalopathy, the case series given below demonstrates that IV thiamine appears efficacious and safe for use
- MOA: Acts on GABA-A receptors produces an increase in the frequency of opening of the chloride ion channel
- Indication: Alcohol withdrawal syndrome and Seizure activity
- Efficacy: Oral benzodiazepines are the best studied and most effective drugs for preventing a severe alcohol withdrawal syndrome
- MOA: Crosses the BBB and enhances the release of GABA but does not act as an agonist on the GABA-a receptor
- Indications: Alcohol withdrawal syndrome and Seizure activity
- Efficacy: Separate analyses of the pregabalin and the placebo group showed a significant reduction in diazepam use from Day 2 to 6 (pregabalin: Z = −2.842, P = 0.004; placebo: Z = −2.916, P = 0.004).
- Chronic alcohol dependence causing decreased erythropoiesis as there is a direct toxic effect of alcohol on the bone marrow
- Anemia can be secondary to poor nutrition and malabsorption syndrome
- Alcoholic gastritis that could have caused a hemorrhage in the stomach leading to loss of blood
- Possibility of liver cirrhosis that could have caused sequestration of RBCs in spleen
- Chronic alcohol consumption since past 30 years (90-180 ml/daily)
- 7 days before admission, had a brief episode of giddiness and one episode of vomiting
- 4 days ago, consumed alcohol and developed giddiness associated with Bilateral Hearing loss, aural fullness tinnitus and 2-3 episodes of vomiting per day.
- Presented to the OPD with Slurring of speech and deviation of mouth
- Anatomical Localisation:
- Infarction in the Right inferior Cerebellar Hemisphere
- Primary Etiology:
- Untreated Hypertension
- Chronic Smoking
- MOA: Blocks 5-HT action on Vagal afferents in GIT
- Indication: Patient had non-projectile vomiting
- MOA: Aspirin exerts direct neuroprotective effects according to recent studies
- Indication: Patient has Cerebellar infarction
- Efficacy: At the acute phase of cerebral infarction, two recent large studies found that the use of aspirin reduces both mortality and the risk of the recurrence of stroke.
https://www.researchgate.net/publication/262926658_Aspirin_and_cerebral_infarction#:~:text=At%20the%20acute%20phase%20of,not%20reduce%20that%20of%20stroke
Atorvastatin:
- MOA: Reduces cholesterol synthesis by inhibiting HMG-CoA reductase
- Indication: The cerebellar infarct could be a cause if ischemic stroke due to Atherosclerosis
- Efficacy: In patients with recent stroke or TIA and without known coronary heart disease, 80 mg of atorvastatin per day reduced the overall incidence of strokes and of cardiovascular events
- MOA: Inhibits P2Y-12 receptors on platelets in-turn inhibiting their aggregation
- Indication: Patient has a possible Ischemic Stroke
- Efficacy: Combination antiplatelet therapy with clopidogrel and aspirin may reduce the rate of recurrent stroke during the first 3 months after a minor ischemic stroke or transient ischemic attack
- 10 years back, had an episode of Quadriplegia
- Quadriparesis since 1 year
- Bilateral Pedal Edema (pitting) since 8 months
- Since 6 days, radiating pain in the left upper limb
- 5 days ago, developed chest pain along with grade 3 dyspnea associated with palpitations
- Dorsal nerve roots of Cervical Vertebrae
- Possible Primary Etiology
- Age > 40 years
- Female who has likely attained menopause may have Osteoporosis
- Degenerative Disc Disease
- Slightly prolonged PR interval
- Flattening and Inversion of T-wave
- Q-T interval prolongation
- Visible U wave
- Mild ST depression
- Loss of Balance, headache and dizziness
- Sudden loss of vision in one or both eyes
- Facial drooping
- Arm or leg weakness
- Slurring of speech
- Mannitol
- Ecosprin
- Atorvastatin
- 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.
- Normal ejection fraction is when anything between 50-70% blood is pumped out
- Borderline ejection fraction when 41-49% blood is pumped out with each contraction
- In reduced ejection fraction, less that 40% of the blood is pumped out
- Coronary Artery Disease
- Non-ischemic dilated Cardiomyopathy
- COPD/Cor pulmonale
- Valvular heart diseases
- Chronic brady or tachy arrhythmias
- Hypertension
- Restrictive Cardiomyopathy
- Chronic constructive pericarditis
- Hypertrophic cardiomyopathy
- Diabetes
- Hypertension
- Older age
- Male patient
- Smoker
- Alcohol consumption
- Inguinal hernia 10 years ago. Got surgery
- First episode of grade 2 dyspnea one year ago
- Facial edema on and off since 2-3 years
- hypertensive since 1 year
- Decreased urine output since 2 days
- Grade 2 dyspnea which progressed to grade 4 since 1 day
- Anuria since the morning of admission
- Atrial Septum
- primary etiology:
- Atrial Septal defect leading to Atrial Fibrillation
- Atrial fibrillation caused stagnation of blood and hence thrombus formation
- Atrial septal defect also caused shunting from left to right atrium causing pulmonary hypertension
- Pulmonary Hypertension caused reversal of shunting and hence increased stagnated pool of blood contributing to thrombus formation and Congestive Cardiac failure
- Torsemide:
-MOA: Blocking Na-K-Cl co transporter in loop of Henle > loss of K, Na and Cl in urine
-Indication:The patient has Congestive Cardiac Failure-Efficacy:Torasemide is a lipophilic anilinopyridine sulphonylurea derivative that acts as a high ceiling loop diuretic and has been used for the treatment of both acute and chronic congestive heart failure (CHF) and hypertension
- Dobutamine:
-MOA: Acts on alpha-1, beta-1 and beta-2 adrenergic receptors. In the heart, the stimulation of these receptors produces a relatively strong, additive inotropic effect and a relatively weak chronotropic effect-Indication: To increase contractility of heart in CCF patients-Efficacy: Dobutamine is a cardiac inotrope useful in the acute treatment of congestive heart failure. Dobutamine improves cardiac output, decreases pulmonary wedge pressure, and decreases total systemic vascular resistance with little effect on heart rate or systemic arterial pressure
- Digoxin
MOA: Na-K ATPase inhibition causing intracellular Ca and hence the contractility
Indication: Patient is suffering from CHF and Atrial fibrillations and therefore has incomplete contractionsEfficacy: Digoxin, also called digitalis, helps an injured or weakened heart pump more efficiently. It strengthens the force of the heart muscle's contractions, helps restore a normal, steady heart rhythm, and improves blood circulation.
- Heparin:
MOA: Produces an anticoagulant effect by inhibiting activated factor X and thrombin and hence prevents fibrin formationIndication: The patient had thrombi in left atrium and left appendages
- Acenocoumarol:
MOA: Vitamin K antagonist, produces anticoagulant effectIndication: oral anticoagulant given as prophylaxis for biatrial thrombusEfficacy: Efficacy of acenocoumarol has been evaluated in atrial fibrillation. Acenocoumarol is effective and safe in all age groups.
- LV dysfunction which developed due pulmonary hypertension which was a cause of Atrial fibrillation
- The Atrial Septal Defect caused shunting of blood, and when pulmonary hypertension developed due to this, that resulted in reversal of shunt causing deoxygenated blood to reach the left atrium which was pumped to the rest of the body
- Hypertension
- NSAID abuse
- Older age (52 years)
- Male gender
- She had heartburn like episodes which subsided without medication since 1year
- She was diagnosed with tuberculosis 7 months ago for which she has completed the course of medication
- She was diagnosed with diabetes 12 years back and with hypertension 6 months back
- She had the first episode of SOB half an hour ago
- ECG taken then upon admission showed NSTEMI(coronary syndrome) and she was given TAB MET XL 25 MG/STAT.
- She was advised to get PCI but she didn’t get it and symptoms subsided and she is doing fine now
- MOA:by blocking beta-1-adrenergic receptors on the cardiac cells
- Indication : ECG was suggestive of NSTEMI
- Efficacy : The use of early β-blocker therapy in acute MI reduces the risks of reinfarction and ventricular fibrillation, but increases the risk of cardiogenic shock, especially during the first day or so after admission.
- MOA : PCI is a non surgical minimally invasive technique in which the balloon catheter widens the coronary artery and a stent is placedtwith the help of angiography
- Indication : NSTEMI
- Efficacy : in immediate invasive strategy (<2hours) indicated in very-high-risk NSTEMI criteria, immediate coronary angiography along with PCI is effective
- Acute ST elevation myocardial infarction (STEMI)
- Non ST elevation acute coronary syndrome
- Stable angina
- Anginal equivalent (eg, dyspnea, arrhythmia, dizziness/syncope)
- Asymptomatic or mildly symptomatic patients with objective evidence of a moderate to large area of viable myocardium or moderate to severe ischemia on noninvasive testing.
- Significant comorbidities (relative contraindication)
- Hemodynamically significant lesion in a vessel serving viable myocardium (vessel diameter >1.5 mm)
- Left main stenosis in a patient who is a surgical candidate
- Diffusely diseased small-caliber artery or vein graft
- Other coronary anatomy not amenable to percutaneous intervention
- There are often risks associated with PCI like blood clots, renarrowing of the coronary artery, bleeding from the site of catheterization .We may push the patient into these risks when the procedure is performed in patients who may not need it or when it can be managed by medication .
- Harms of overtretment are psychological stressors, morbidity, unnecessary surgical complications as seen after small renal masses resection surgeries
- Research on overtesing and overtretment is important because there are downfalls to overtesing and overtretment .
- Huge amount of healthcare money is wasted on unnecessary treatment and testing and more testing and treatment is not linked to better outcome and may become worse sometimes
- Dragging type of retrosternal chest pain on the right side, 3 days back.
- Dizziness present
- Inferior ventricular wall of the myocardium.
- TAB. ASPIRIN 325 mg:
MOA: ASPIRIN inhibits platelet aggregation by interfering with thromboxane A2 in platelets, caused by COX-1 inhibition. Thromboxane A2 is an important lipid responsible for platelet aggregation, which can lead to clot formation and future risk of heart attack or stroke
INDICATION: Reducing the risk of cardiovascular death in suspected cases of myocardial infarction (MI)EFFICACY: a low-dose aspirin each day for at least 10 years can lower your risk of cardiovascular disease by as much as 10%. A significant decrease in the risk of serious cardiovascular events, including nonfatal myocardial infarction, stroke, or cardiovascular death, was seen with use of aspirin. Odds ratios (ORs) ranged from 0.85 (95% CI 0.79–0.92) to 0.90 (95% CI 0.85–0.96).
- TAB ATORVASTATIN 80mg:
MOA: .It is a competitive inhibitor of the enzyme HMG-CoA reductase, which is an enzyme involved in cholesterol systhesis.INDICATION: To prevent cardiovascular events in patients with cardiac risk factors and/or abnormal lipid profiles. Its used as a preventive agent for non-fatal myocardial infarction, fatal and non-fatal stroke, revascularization procedures, hospitalization for congestive heart failure and angina in patients with coronary heart disease.EFFICACY: Clinical studies with this agent have shown that LDL cholesterol concentrations may be decreased by up to 61% at doses of 80 mg, and triglycerides may be reduced by 46%.
- TAB CLOPIDOGREL 300mg PO/STAT
MOA: The active form of clopidogrel is a platelet inhibitor that irreversibly binds to P2Y12 ADP receptors on platelets. This binding prevents ADP binding to P2Y12 receptors, activation of the glycoprotein GPIIb/IIIa complex, and platelet aggregation.
INDICATION: Clopidogrel is indicated to reduce the risk of myocardial infarction for patients with non-ST elevated acute coronary syndrome (ACS), patients with ST-elevated myocardial infarction, and in recent MI, stroke, or established peripheral arterial disease.EFFICACY: Clopidogrel had the greatest effect on reducing the rate of an occluded infarct-related artery (18.4% placebo vs 11.7% clopidogrel; 41% odds reduction; 95% CI: 0.28–0.52; p<0.001) and there was a consistent reduction in recurrent MI (3.6% placebo vs 2.5% clopidogrel; 30% odds reduction; p=0.08)
- INJ HAI 6U/IV STAT ( Human ACTRAPID Injection)
MOA: The blood glucose lowering effect of ACTRAPID (fast - acting insulin) is due to the facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver.INDICATION: For treatment of diabetes mellitus. Its used in thscase as it is fast acting and here the patient requires immediate control of hyperglycemia.EFFICACY: A clinical trial in a single intensive care unit treating hyperglycaemia (blood glucose above 10 mmol/L) in 204 diabetic and 1344 non-diabetic patients undergoing major surgery showed that normoglycaemia (blood glucose 4.4 - 6.1 mmol/L) induced by intravenous Actrapid reduced mortality by 42%
CASE I:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
QUESTIONS & ANSWERS:
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?
A.) EVOLUTION OF SYMPTOMATOLOGY:
1) 5yrs ago patient developed abdominal pain along
with vomiting, which subsided on treatment in a local hospital.
ANATOMICAL LOCALIZATION :
1. Body of the pancreas.
2. Left basal lung.
3. Sub-hepatic region
4. Stomach
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?
A. 1) ING. MEROPENAM
MEROPENEM is carbapenem
antibiotic approved by the US FDA, for the treatment of complicated intra
abdominal infections. Like other carbapenems, meropenem is
stable against chromosomal and extended-spectrum beta-lactamases. In patients
with moderate to severe intra-abdominal infections, empirical
monotherapy with meropenem achieved clinical response rates
ranging from 91 to 100% in 7 randomised comparative trials.
https://www.researchgate.net/publication/12294847
2) ING. METROGYL
Eight
studies comparing metronidazole combination therapies and carbapenem were
included. No difference was found between combined therapy with metronidazole
and carbapenem regarding clinical success (odds ratio [OR] = 1.31; 95%
confidence interval [CI], .75-2.31), bacteriological eradication (OR = 1.27;
95% CI, .84-1.91), all-cause mortality (OR = 0.61; 95% CI, .37-1.00), or
drug-related adverse events (OR = 0.58; 95% CI, .18-1.88). Sensitivity analyses
found similar results.
Combined
therapy with metronidazole is as effective and safe as carbapenem in treatment
of cIAI. Therefore, combined therapy with metronidazole offers an effective
alternative to carbapenem with low risk of drug resistance.
https://pubmed.ncbi.nlm.nih.gov/27704002/
3) ING. AMIKACIN
Administration of amikacin in intra abdominal sepsis has become increasingly widely used because of the appropriate efficacy of this agent against the invasive gram negative pathogens as well as the lack of existing antibiotics.
4) ING. OCTREOTIDE
Octreotide being the
long-acting analogue of somatostatin, inhibits exocrine secretions of pancreas.
It also has direct anti inflammatory and cytoprotective effects.
The overall efficiency of observation group was
significantly higher than that of control group (83.3% vs 65.0%, P < 0.05).
And abdominal pain relief time, decompression
time, surgical intervention rate, length of stay and mortality rate of
observation group (1.9 ± 0.9 d, 6.3 ± 2.2 d, 1.7%, 11.8 ± 0.5 d, 5%) were
significantly lower than those of control group (3.6 ± 0.7 d, 10.4 ± 3.1 d,
8.3%, 23.7 ± 2.1 d, 15.0%) (P < 0.05).
After treatment, the levels of blood amylase,
white blood cell (WBC), C-reactive protein (CRP) and interleukin 6 (IL-6) of
observation group were significantly lower than those of control group (P <
0.05).
And the incidences of such complications as
acute respiratory distress syndrome (ARDS), acute renal failure and shock of
observation group (10.0%, 5.0%, 13.3%) were significantly lower than those of
control group (36.7%, 21.7%, 33.3%) (P < 0.05).
https://pubmed.ncbi.nlm.nih.gov/26178495/
CASE II:
B) Link to patient details:
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
A) With severe pancreatitis there are a lot of inflammatory chemicals that are secreted into the blood stream. These chemicals create inflammation throughout the body, including the lungs. As a result, a person may experience an inflammatory type of reaction in the lungs called ARDS. Specifically, the small air sacs inside the lungs called the alveoli can get inflamed and become filled with fluid causing acute respiratory distress syndrome.
Acute pancreatitis can cause chemical changes in your body that affect your lung function, causing the level of oxygen in your blood to fall to dangerously low levels.
https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227
2) Name possible reasons why the patient has developed a state of hyperglycemia.
A) Some pancreatic tissue dies during acute pancreatitis
episodes, which increase the risks for developing diabetes. This might be the reason for the development of the hyperglycemia in this patient.
https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227/
3) What is the reason for his elevated LFTs? Is there a
specific marker for Alcoholic Fatty Liver disease?
A.) Elevated alanine aminotransferase (ALT)
and aspartate aminotransferase (AST) levels reflect nonspecific hepatocellular
damage. In NAFLD/NASH, aminotransferase levels may be elevated two to four
times over the upper limit of normal , with ALT being higher than AST, in
contrast to alcoholic steatohepatitis. However, in the absence of advanced
disease, routine liver function tests are either normal or typically show only
mild elevations in aminotransferase levels, with alkaline phosphatase and
gamma-glutamyl transferase (GGT) 1.5 to three times the upper limit of normal.
Several studies involving hepatology
clinic patients undergoing liver biopsy and morbidly obese individuals
undergoing bariatric surgery have found ALT levels to be higher in the presence
of NASH than in those with simple steatosis, although this has not been
universally observed.
Therefore, Alanine aminotransferase (ALT) could be the specific marker for alcoholic liver disease, but extensive reasearch into this topic is very much needed.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4277175/
4) What is the line of treatment in this patient?
A. Here, the patient is being given symptomatic treatment, with IV fluids and basic drugs like Paracetamol, Ondansetron, and Tramadol.
No surgical intervention is needed in this patient as of
now. But pleural tapping is being done so as to assess the pleural effusion
fluid biochemically.
CASE III:
C) Link to patient details:
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
1.) What is the most probable diagnosis in this patient?
A. A.) It most probably looks like hollow viscus perforation, attributed to intestinal obstruction following which patient must have gone int shock, causing multiple organ failure , even though in the starting stage.
INTESTINAL OBSTRUCTION ----> HOLLOW VISCUS PERFORATION
----> SHOCK ----> MULTIORGAN FAILURE
2) What was the cause of her death?
3) Does her NSAID abuse have something to do with her
condition? How?
A) NSAID abuse could have caused this condition:
NSAID ABUSE (for 4 years) ----> ULCER IN GIT ----> PERFORATION
----> INTERNAL HAEMMORHAGE ( hence haemorraghic aspirate) ---->
SHOCK ----> MULTIORGAN FAILURE.
5) NEPHROLOGY AND UROLOGY
CASE I:
A) Link to patient details:
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
Questions:
1. 1)what could be the reason for his SOB?
A)During TURP, the wide plexus of venous sinuses is often
opened and the absorption of the irrigation fluid causes a group of symptoms
and findings that is called TURP syndrome.2 Absorption of the irrigation fluid (2000 ml or more)
may lead to TURP syndrome which causes headaches, anxiety, confusion, dyspnoea,
arrhythmia, hypotension and seizures and can be fatal if not treated. The
symptoms of TURP are generally caused by an excessive fluid load in
circulation.
Reference :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4543890/
2. why does he have intermittent episodes of drowsiness ?
A)It might be due to uremic encephalopathy
Reference :https://www.ncbi.nlm.nih.gov/books/NBK564327/
3. why does he complain of fleshy mass like thing passing in the urine?
A)It might be the blood clot or the scab falling off the prostate during healing after the turp surgery
https://www.nhs.uk/conditions/transurethral-resection-of-the-prostate- turp/recovery/
4. what are the complications of turp he may have had?
A) The complications of turp:
- Urinary tract infection
- Passing of blood clots in urine
- TURP syndrome
https://www.medicalnewstoday.com/articles/321190#complications
B) Link to patient details:
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
Questions
1.Why
is the child excessively hyperactive without much of social etiquettes ?
A)The child might have had attention deficient hyperactive disorder (ADHD) because of which he may be hyperactive and due to his less attention span he may be impulsive and may not be able to interact with others much so he may not have much social etiquettes.
2. Why doesn't the child have the excessive
urge of urination at night time?
A)The child may be having psychosomatic urge to
urinate duringthe day but this will not be present during sleep as he will not
be conscious
3. How would you want to manage the patient to
relieve him of his symptoms?
A)Urinating on
schedule and gradually lengthening the time between bathroom visits
Medication. Drugs that
relax bladder like botox injection
Anti anxiety drugs
Nerve stimulation. This includes some of the latest treatment options for OAB. They sometimes may help when there is no improvement with medications
6)INFECTIOUS DISEASE (HI Virus, Mycobacteria, Gastroenterology, pulmonology)
A) Link to patient details:
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
A)
• Cough on taking food and liquid.
• Difficulty in swallowing.
• Weight loss of 10kg.
Physical findings suggestive of tracheooesophageal fistula:
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
A) The suppression of CD4 T cells by HIV causes a decrease in the body's normal response to certain infection.
If the CD4 count rapidly increases (due to effective treatment of HIV, or removal of other causes of immunosuppression), a sudden increase in the inflammatory response produces nonspecific symptoms such as fever, and in some cases a worsening of damage to the infected tissue.
There are two common IRIS scenarios. The first is the “unmasking” of an occult opportunistic infection. The second is the “paradoxical” symptomatic relapse of a prior infection despite microbiologic treatment success. Often in paradoxical IRIS, microbiologic cultures are sterile. In either scenario, there is hypothesized reconstitution of antigen-specific T cell-mediated immunity with activation of the immune system following HIV therapy against persisting antigen, whether present as intact organisms, dead organisms, or debris.
To prevent IRIS , ART treatment is given before CD4 cells count go down below 100cells/ul.
We should prevent advanced immunosuppression.
https://en.m.wikipedia.org/wiki/Immune_reconstitution_inflammatory_syndrome#:~:text=Immune%20reconstitution%20inflammatory%20syndrome%20(IRIS,paradoxically%20makes%20the%20symptoms%20of
https://www.infectiousdiseaseadvisor.com/home/decision-support-in-medicine/infectious-diseases/immune-reconstitution-inflammatory-syndrome/#:~:text=How%20can%20immune%20reconstitution%20inflammatory,greater%20than%20100%20cells%2FuL.
7) Infectious disease and Hepatology:
CASE I:
Link to patient details:
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
Q&A:
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 ?
A. In this
case, LOCALLY-BREWED ALCOHOL can be the possible cause of liver abscess because
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. Following alcoholism,
poor economic status & malnutrition also plays a vital role as predisposing
factors in the formation of liver abscess. Among alcoholism also, consuming
locally prepared alcohol plays a vital role, but the reason is still been
unknown.
2. What is
the etiopathogenesis of liver abscess in
a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
A. 1.] Factors
influencing the association could be related to the:
- Pathogen
- Contents of beverages
- Status of the liver
- Immunity of the host.
- Large infective dose of Entamoeba histolytica or Other bacterial pathogens ingested with the unhygienically brewed beverage.
- Nutritional status of the population
- Poor sanitation
- Alcohol-induced hepatic dysfunction
- Possible suppression of amoebistatic immune mechanisms by substances in the beverages could also be attributed in the mechanism.
2.] Mechanisms responsible:
- Hepatic damage by alcohol,
- Lowered body resistance and
- Suppression of liver function due to poor nutritional status of habitual consumers of alcohol,
- Increased presence of amoebae in the liquor prepared locally with poor regard to aseptic procedures, and
- Depression of immune mechanisms in chronic alcoholics.
3. Is liver abscess more common in right lobe ?
A. Liver abscess is more common in right lobe because of more blood supply to the right lobe relatively. Due to this fact pathogens are carried in increased proportions to the right lobe.
4.What are
the indications for ultrasound guided aspiration of liver abscess ?
A. INDICATIONS OF LIVER ABCESS DRAINAGE:
1) If the abcess is large ( 5cm or more) because it has more
chances to rupture.
2) If the abcess is present in left lobe as it may increase the
chance of peritoneal leak and pericardial leak.
3) If the abcess is not responding to the drugs for 7 or more
days
CASE II
B) Link to patient details:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
Q&A:
1) Cause of liver abcess in this patient ?
A) Most amoebic infections are caused by Entamoeba histolytica. The pyogenic abscesses are usually polymicrobial, but some organisms are seen more commonly in them, such as E.coli, Klebsiella, Streptococcus, Staphylococcus, and anaerobes.
While the incidence is low, it is essential to understand the severity of these abscesses because of the high mortality risk in untreated patients.
If the cause is infectious, the majority of liver abscesses can be classified into bacterial (including amebic) and parasitic sources (including hydatiform cyst).
The right lobe is more commonly affected lobe.
2) How do
you approach this patient ?
A.Treatment along with rationale:
- INJ. ZOSTUM 1.5mg IV (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)
- INJ. METROGYL 500mg IV TID
Metrogyl has the drug called METRONIDAZOLE [Antibiotic]: For amoebic cause
- INJ. OPTINEURIN 1amp in 100ml NS IV OD:
Optineurin is a multivitamin drug {A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement
- TAB. ULTRACET 1/2 QID:
Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and fever
- TAB. DOLO 650mg sos, given for fever and pain
* Here ; due to medical therapy his symptoms subsided and clearly we can see it in usg reports ( liquefaction has occured) meaning abcess responded to our medical therapy.
* We donot aspirate the pus since it is self resolving and aspiration is associated with several other complications.
3) Why do we
treat here ; both amoebic and pyogenic liver abscess?
A. Empirical antibiotic coverage is essential when the organism is unknown. The antibiotics
should cover Enterobacteriaceae, anaerobes, streptococci, enterococci, and
Entamoeba histolytica. Such antibiotic regimens include cephalosporins plus
metronidazole, Beta-lactam Beta-Lactamase inhibitor plus metronidazole, or
synthetic penicillins plus aminoglycosides and metronidazole.
Metronidazole should cover Entamoeba histolytica. The
duration of treatment varies but is usually from two to six weeks. After
initial intravenous treatment, the oral route can be used safely in most cases
to complete the course.
4) Is there
a way to confirm the definitive diagnosis in this patient?
A. As the
condition subsided with empirical treatment in this patient, there is no need
of a definitive diagnosis in this patient.
But a
definitive diagnosis can be achieved if the abscess is aspirated and sent for
culture.
A) Link to patient details:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Questions :
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?
• Evolution of symptomatology:
Day 1-Patient took covid vaccination, on that night patient had high grade fever assosciated with chills and rigor , relieved on medication
Day 4 – Patient had fever assosciated with chills and rigor but not relieved by medication.
Day 11- patient complains of generalised oedema, facial puffiness, periorbital edema.
Day 17- Altered state , facial puffiness, periorbital oedema and weakness of right upper and lower limb.
• Anatomical localization of problem:
Frontal and temporal lobe of brain - infarcts
Orbit
Oral cavity : eshcar extending from hard palate to lip
Left nasal cavity
• Primary etiology of patients problem
Mucormycosis infection causing rhino-orbito-cerebral mucormycosis.
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?
• Azoles.Itraconazole is the only marketed azole drug that has in vitro activity against Mucorales. There are case reports of successful therapy with itraconazole alone .However, as mentioned above, itraconazole prophylaxis has been described as a risk factor for breakthrough mucormycosis .
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
A) • Covid 19 infection among diabetic patients in whom there is lower immunity.
• Increased dose of steroid usage and also because of lower availability of remedesivir , tocilizumab leading to dependance on steroids for treatment.
• Use of ordinary water instead of sterile water in humidifiers.
• Prolonged ICU stay.
CASE I:
covid 19 with co morbidity (Pulmonology/Rheumatology)
https://nikhilasampathkumar.blogspot.com/2021/05/covid-pneumonia-in-pre-existing-case-of.html
Possible questions:
1) How does the pre-existing ILD determine the prognosis of this patient?
A)• Patients with ILD have diminished pulmonary reserve and impaired gas exchange due injury to alveolar epithelium.
• Prognosis of covid19 patients with preexisting ILD is significantly worse than non ILD patients.
2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism?
• Studies have shown that steroids used for treatment did not worsen the prognosis of rheumatoid arthritis.
https://www.health.harvard.edu/blog/does-lupus-or-arthritis-affect-your-prognosis-if-you-get-covid-19-2020110921230#:~:text=There%20was%20some%20good%20news,prognosis%20for%20the%20arthritis%20patients.
• Couldn’t find studies,how steroids affect hypothroidism.
3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?
• Not sure about whether this patient has increased risk for post covid autoimmune response.
4) Why was she prescribed clexane (enoxaparin)?
• IL6 is involved in cytokine storm,enoxaparin has IL6 binding properties thus preventing cytokine storm.
• Prevention of infection by decreasing virus cell entry and hence viral load
• Prevention of activation of coagulation cascade
• Prevention of venous thromboembolism
Covid 19 with Diabetes
Link to the patient case report log:
https://nehapradeep99.blogspot.com/2021/05/a-50-year-old-female-with-viral.html
Questions:
1) Since patient didn't show any previous characteristic diabetes signs, did the Covid-19 infection aggravate any underlying condition and cause the indolent diabetes to express itself? If so what could be the biochemical pathways that make it plausible?
A)The exact pathology of new onset diabetes in COVID-19 patients is not known, but this could be a possible explanation. Beta cells in the pancreas contain a significant number of so-called ACE2 receptors. These receptors are believed to be where the spike protein from the coronavirus attaches to cells. Beta cells produce insulin. It is theorised that a coronavirus infection, which affects the ACE2 receptors, might also damage beta cells in the pancreas and hence precipitating diabetes.
2) Did the patient's diabetic condition influence the progression of her pneumonia?
A)Diabetic subjects may have increased susceptibility to pneumonia for several reasons. They are at increased risk of aspiration, hyperglycemia, decreased immunity, impaired lung function, pulmonary microangiopathy, and coexisting morbidity.
3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?
A)D-dimer is a fibrin degradation product, elevated D-dimer levels have been associated with disease severity and mortality trends. Several studies from Wuhan have shown elevated D-dimer in COVID-19 patients is associated with higher mortality.
There is not yet a consensus as to how D-dimer levels should be used for management and/or monitoring of COVID-19 patients. Checking D-dimer on initial presentation in the emergency department, urgent care facility or outpatient clinic is appropriate.
CASE III:
Covid 19 Severe
Link to the complete case report log:
https://143vibhahegde.blogspot.com/2021/05/covid-in-26-yo-female.html
Questions:
1. Why was this patient given noradrenaline?
A)The patient following AKI along with the viral infection could have gone under septicemic shock. This would create a severe hypotensive state. To correct this, Noradrenaline was administered.
2. What is the reason behind testing for LDH levels in this patient?
A)LDH is often used as a marker of tissue breakdown as LDH is abundant in red blood cells and can function as a marker for hemolysis. It can also be used to diagnose renal infarction. So as the patient has both covid infection and renal complications, LDH works as a diagnostic marker.
3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
A)As biPAP is not intended for full ventilatory support and is contraindicated in the patients who are unable to maintain spontaneous breathing, invasive mechanical ventilation provides more support to these patients. Once the patient starts to recover and maintain spontaneous breathing, he can be shifted onto an NIV.
CASE IV:
Covid 19 Mild
Link to the case report log:
https://gsuhithagnaneswar.blogspot.com/2021/05/29-year-old-male-patient-with-viral.html?m=1
Questions:
1. Is the elevated ESR due to covid related inflammation?
A)If there is inflammation following a covid infection, then elevated ESR can be a possible cause of it. During an inflammatory process, increased levels of fibrinogen is released into the blood, causing them to stick together and form rouleaux.
2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization?
A) The patient was probably admitted as it was a long-standing case of Covid and the patient’s dyspnea had progressed to grade 3 with further exaggeration of his other symptoms also.
If the patient had opted for home isolation, then an emergency could not have been taken care of. And as the patient’s condition was deteriorating with each following day, hospital admission was advisable
As the steroidal therapy given for covid could have disrupted his immune system, admission in a hospital makes him more susceptible to the nosocomial infections.
CASE V:
Covid 19 and comorbidity (Altered sensorium, azotemia, hypokalemia)
Link to the case report log:
https://anuragreddy72.blogspot.com/2021/05/case-discussion-on-hypokalemic-periodic.html
1)What was the reason for coma in this patient?
A) Hypoxic encephalopathy And Viral encephalopathy probably produced the comatose condition of this patient.
2)What were the competency gaps in hospital 1 Team to manage this intubated comatose patient that he had to be sent to hospital 2? Why and how did hospital 2 make a diagnosis of hypokalemic periodic paralysis? Was the coma related?
A) Hypokalemic periodic paralysis diagnostic tests??
3)How may covid 19 cause coma?
A) Infarct in the brain could have developed secondary to embolism which could have been the reason for his coma.
It could also have occurred secondary to hypoxic damage due to low O2 saturation which was a result of COVID infection.
CASE VI:
Severe Covid 19 with altered sensorium
Link to the case report log:
https://vijaykumarkasturi.blogspot.com/2021/05/65-years-old-male-with-viral-pneumonia.html
Questions:
1. What was the cause of his altered sensorium?
A)The most probable cause of altered sensorium in this patient can be Hypoxic encephalopathy due to severe fall in SpO2 of the patient.
It can also be Viral Encephalopathy post covid-19 infection
Another possibility is the Hyperglycaemic condition that can cause delirium and even coma might develop. But that would need the evidence of diabetic ketoacidosis.
2. What was the cause of death in this patient?
A)Hypoxic encephalopathy can be the main cause of the Patient’s death after there was ischemic damage done to the neural tissue.
It could also be due to pulmonary thromboembolism due to Covid infection
CASE 7
Covid 19 Moderate with ICU psychosis
- hyperactive
- hypoactive
- mixed type
- age
- Presence of any previous psychological illness
- acute or chronic illness
- renal disease or impairment
- diagnosis of sepsis
- smoking
- acute respiratory distress
- copd
- absence of daylight exposure
- Haloperidol
- Antipsychotics
- wearing a mask when near them
- sanitising all the household items
- maintaining personal hygiene
- regular drug administration as prescribed by the physician
- frequent monitoring of SpO2 levels.
- Elevated pressure in the eyes (glaucoma)
- Clouding of the lens in one or both eyes (cataracts)
- A round face (moon face)
- High blood sugar, which can trigger (New onset diabetes) or worsen diabetes
- Increased risk of infections, especially with common bacterial, viral and fungal(mucormycosis) microorganisms.
- Thinning bones (osteoporosis) and fractures
- Suppressed adrenal gland hormone production that may result in a variety of signs and symptoms, including severe fatigue, loss of appetite, nausea and muscle weakness
- Thin skin, bruising and slower wound healing
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- Innate immunity
- adaptive immunity
- past exposure to any of these endemic viruses (HCoV-229E, HCoV NL-63, HCoV-OC4, HCoV-HKU1) which show sequence homology of structural proteins in SAR-Co V and MERS-CoV. Thus, the possibility of a protective cross-immunity in the Indian population against COVID-19 cannot be ignored in explaining a rather mild effect of the current coronavirus pandemic in India in comparison to that in Europe and the USA.
- Malaria endemicity might have a role to play. It is plausible that persons in malaria-endemic zones, which may also be endemic for several tropical pathogens including viruses, have recurrent cytokine fluctuations in response to minor and subclinical infections. These recurrent fluctuations may have a de-sensitizing effect on the body’s immune system, which prevents an uncontrolled and detrimental immune response and thus severe clinical disease in SARS-CoV-2 infection.
- Cytokine storm destroying the pancreatic beta cells, leading to lower levels of insulin.
- Virus entering through ACE-2 receptors in the lung tissue, and destroying these receptors which are also present in pancreatic tissue, thereby causing decreased levels of insulin, thereby causing hyperglycemia.
- lets not forget the STEROIDS, which induce hyperglycemia by various mechanisms, not only worsening the condition of already diabetic patient, but also causing NEW ONSET DIABETES.
Moderate to severe covid with prolonged hospital stay:
https://93deepanandikonda.blogspot.com/2021/05/42-years-female-patient-with-viral.html
Questions :-
1) What are the potential bioclinical markers in this patient that may have predicted the prolonged course of her illness?
A)• CRP
Rise in CRP indicate a more severe outcome later and more reliable for early identification of case severity
• NLR(Neutrophil-to-lymphocyte-ratio)
High NLR suggest more severe outcome
• Lactate dehydrogenase
High levels of LDH suggest more necrosis of lung tissue and pneumonia and severe disease that causes prolonged stay
• D-dimer
D-dimer is measure of coagulation and fibrinolysis activity. With increase in D-dimer there is increased risk of mortality and morbidity
Reference : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219356/#!po=20.1220
CASE 13:
Severe covid with first diabetes
Link to Case report log :
https://vignatha45.blogspot.com/2021/05/58-years-female-patient-with-viral.html
1.What are the consequences of uncontrolled hyperglycemia in covid patients?
A)• Increased hospital stay
• Increased risk of mortality
• Increased risk of complications
Reference : https://care.diabetesjournals.org/content/43/8/1695#:~:text=A%20retrospective%20study%20of%20451,or%20uncontrolled%20hyperglycemia%20(13).
2. Does the significant rise in LDH suggests multiple organ failure?
A) Yes, Extremely high levels of LDH isoenzymes can indicate multi organ failure
Reference https://www.healthline.com/health/lactate-dehydrogenase-test#test
3.What is the cause of death in this case?
A)• The patient has elevated SGPT, SGOT and ALP which indicate there is liver damage
• SGOT:170 IU/lit
• SGPT:444 IU/lit
• ALP:303 IU/lit
• Serum LDH was very high indicating tissue damage
serum LDH:835 IU/lit
• CRP is positive
• D-dimer level is elevated D-dimer:560ng/ml
• Blood urea is very high indicating failing kidneys
Blood urea:87mg/dl
So the possible cause of death is due to liver and kidney failure along with coagulation and fibrinolysis or multiple organ failure
CASE 14
Long covid with sleep deprivation and ICU psychosis
Link to Case report log:
https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html
Questions:
1)Which subtype of ICU psychosis did the patient land into according to his symptoms?
A) ICU psychosis can be assessed by Confusion Assessment Method (CAM)-ICU-7 delirium severity scale.
Reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5392153/#:~:text=The%20final%20CAM%2DICU%2D7,6%2D7%3A%20severe%20delirium.
2)What are the risk factors in the patient that has driven this case more towards ICU pyschosis?
A)• Prolonged stay at hospital and he has changed 3 different hospitals which might have caused anxiety in him
• He was isolated environmentally which may be a reason
3)The patient is sleep deprived during his hospital stay..Which do u think might be the most propable condition?
A)
A) Sleep deprivation causing ICU pyschosis
B) ICU psychosis causing sleep deprivation
• During ICU stay, the lights, machines beeping, waking up to take the medicines may impact the sleep of the patient and this might also be a cause for ICU psychosis and
• The patient due to ICU psychosis may be in a state of delirium talking to himself not oriented to time which might be the most probable condition
4) What are the drivers toward current persistent hypoxia and long covid in this patient?
• Pneumonia secondary to Covid 19 may drive towards persistent hypoxia after being Covid negative
• Groundglass appearance of nearly 75% of both lungs
• Elevated LDH, CRP,D-dimer all are risk factors for prolonged Covid infection
References : https://link.springer.com/article/10.1007/s12028-019-00795-4
CASE 15
CASE 16
Mild to moderate covid with hyperglycemia
https://vaishnavimaguluri138.blogspot.com/2021/05/viral-pneumonia-secondary-to-covid-19.html
QUESTIONS:
1. What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?
A) The possible mechanisms of COVID-19 causing abnormal glucose metabolism include islet β cell damage and insulin resistance. Previous studies have reported that some viruses can directly cause pancreatic β-cell damage [11], [12], and angiotensin converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor has higher expression in pancreatic endocrine tissues than in exocrine tissues
Reference https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7233217/#!po=39.1892
2. What is the frequency of this phenomenon of New Onset Diabetes in Covid Patients and is it classical type 1 or type 2 or a new type?
A) A better term would be " transient hyperglycemia ". The new onset diabetes is a type -2 form and it is called so only when the hyperglycemia continues to exist even after the steroids are tappered.
3. How is the prognosis in such patients?
A) Usually, the prognosis is affected only if the hyperglycemia isn't monitored. monitoring the rise of sugars and treating them immediately helps the patients to recover faster.
4. Do the alterations in glucose metabolism that occur with a sudden onset in severe Covid-19 persist or remit when the infection resolves?
A) Genrally, the alterations of the glucose metabolism revert to normal after the steroid therapy is stopped.
If, the alterations persist, we consider it as type-2 diabetes mellitus, which can be treated appropriately.
5) Why didn't we start him on Oral hypoglycemic agents earlier?
A) Might be because he was non diabetic and they did not suspect diabetes in him.
Covid 19 with hypertension comorbidity
https://prathyushamulukala666.blogspot.com/2021/05/a-62-year-old-male-patient-with-fever.html
Questions:
1)Does hypertension have any effect to do with the severity of the covid infection.If it is, Then how?
A)Yes,covid infection in hypertensives can lead to severe infection.
• ACE2 is a modulator of the RAAS. The end product of the RAAS, angiotensin II, is a key vasoactive hormone that binds to angiotensin II receptor type 1 (AT1) located in the heart, lungs, blood vessels, kidneys, and adrenal glands, and it plays a central role in myocardial hypertrophy and fibrosis, inflammation, vascular remodeling, and atherosclerosis , by this binding it increases blood pressure. ACE2 is expressed in many human tissues including the nasal epithelium, heart, kidneys, and lungs, and inactivates angiotensin II diminishing its vasoconstrictive and myoproliferative effects.
SARS-CoV-2 binds to the ACE2 receptor via its spike protein to allow entry into host cells. This complex is endocytosed leading to down-regulation of ACE2 and resulting in local accumulation of angiotensin II. Severe respiratory illness is a hallmark of COVID-19 and a primary cause of morbidity- and mortality-local activation of the RAAS is proposed as a mechanism for severe lung injury.
2)what is the cause for pleural effusion to occur??
A) Infection causes local inflammatory reaction resulting in increased capillary microvascular permeability and a rapid outpouring of fluid containing inflammatory cells into the pleural space.
Covid 19 with mild hypoalbuminemia.
https://meesumabbas82.blogspot.com/2021/05/a-38-yo-male-with-viral-pneumonia.html
QUESTIONS:
1.What is the reason for hypoalbuminemia in the patient?
A)• It may be due to pulmonary capillary leakage in lungs , in response to epithelial endothelial damage due to covid infection.
•
https://pubmed.ncbi.nlm.nih.gov/33411411/2. What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?
2)What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?
Answer:
Yes, what the patient is experiencing is known as viral exanthem which is one of the cutaneous manifestation of COVID-19.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7549735/
3. What is the reason for Cardiomegaly?
A)• Direct Myocardial Cell Injury
The interaction of SARS-CoV-2 with ACE2 can cause changes to the ACE2 pathways, leading to acute injury of the lung, heart, and endothelial cells. A small number of case reports have indicated that SARS-CoV2 might directly infect the myocardium, causing viral myocarditis. However, in most cases, myocardial damage appeared to be caused by increased cardiometabolic demand associated with the systemic infection and ongoing hypoxia caused by severe pneumonia or ARDS
https://www.ncbi.nlm.nih.gov/books/NBK556152/
4. What other differential diagnoses could be drawn if the patient tested negative for covid infection?
A)• Influenza
• Mycoplasma pneumonia
• Parainfluenza
• Respiratory syncytial virus
• Streptococcus pneumonia
• Other viral or bacterial pneumonia.
5. Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?
A)• It is well known that D-dimer are produced during fibrin breakdown and serve as a marker of fibrinolytic activity. A relationship between proinflammatory cytokines and markers of activation of the coagulation cascade, including D-dimer, has been demonstrated in critical patients or patients with sepsis .There is also evidence that under inflammatory conditions, the alveolar haemostatic balance is shifted towards a predominance of prothrombotic activity .In addition, pro-inflammatory cytokines may be involved in endothelial injury, and may activate coagulation and inhibit fibrinolysis in patients with severe sepsis.
• D-dimer can be elevated such as in pregnancy, inflammation, malignancy, trauma, liver disease (decreased clearance), heart disease, sepsis or as a result of hemodialysis, CPR or recent surgery)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7286212/#:~:text=It%20has%20been%20reported%20that,patients%20with%20good%20clinical%20prognosis
Covid 19 with first time diabetes .
https://srilekha77.blogspot.com/2021/05/a-48-year-male-with-viral-pneumonia-due.html
Questions:
1)Can usage of steroids in diabetic Covid patients increases death rate because of the adverse effects of steroids???
A)There is still no proper studies undertaken , I couldn’t find any results that have been yet published on steroid adverse effect increases death rate among covid patients
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7391982/
2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically???
A)• In covid patients, immune system is reacting very strongly to the pneumonia, and the lungs are full of immune cells that produce cytokines. In turn, these cytokines act on liver to make clotting proteins. The inflammatory mechanism leads to what we call a “prothrombotic state.”
• The main clotting protein in the blood is fibrinogen. It’s soluble, and we have 2–4 grams per liter in your blood.
• The clotting factors switch soluble fibrinogen to insoluble fibrin, and that is the clot.
• The level is 2–4 grams per liter in most people. If you are pregnant, or as you get older, the levels get higher. They might go up to 5, 6, or even 7 [grams per liter].
But in COVID-19 We are seeing levels of 10, even 14 grams per liter.
And in covid 19 there is clotting occuring even in the tiny blood vessels which is not getting disolved with the normal dose anticoagulants which may increase chances of dying.(MAY BE INCREASING DOSE CAN PREVENT DEATH).
https://www.medicalnewstoday.com/articles/blood-thinners-may-protect-against-covid-19-complications#Several-study-limitations
3)Does chronic alcoholism have effect on the out come of Covid infection???? If yes,how??
A)Yes,chronic intake of alcohol alters the body's immune mechanism.
Chronic ethanol abuse almost doubles the risk of developing acute respiratory distress syndrome . Following are the mechanisms:
- reducing the number of T lymphocytes - by preventing proliferation and by altering cell turnover;
- favoring a pro-inflammatory status through an increased level of proinflammatory cytokines, such as tumor necrosis factor alfa (TNF α) and interleukins 1 and 6 (IL-1, IL-6);
- decreases the function and number of NK (Natural Killers) cells responsible for removing infected or malignant cells;
- disturbance of macrophage functions in the lung alveoli;
- damage to the respiratory ciliated cells which plays an essential role in filtering pathogenic microorganisms.
Severe Covid with Diabetes
https://sudhamshireddy.blogspot.com/2021/05/a-65-year-old-female-with-fever.html
Questions-
1.What can be the causes of early progression and aggressive disease(Covid) among diabetics when compared to non diabetics?
A)• In human monocytes, elevated glucose levels directly increase SARS-CoV-2 replication, and glycolysis sustains SARS-CoV-2 replication via the production of mitochondrial reactive oxygen species and activation of hypoxia-inducible factor 1α.Therefore, hyperglycaemia might support viral proliferation. In accord with this assumption, hyperglycaemia or a history of T1DM and T2DM were found to be independent predictors of morbidity and mortality in patients with SARS-COV-2.
• Also there is altered immune system in diabetics.
https://www.nature.com/articles/s41574-020-00435-4
2. In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?
A)• Two experimental agents (dexamethasone and hydroxychloroquine) have shown some promise as treatment agents.
• Combined treatment with these two agents might be more beneficial than either agent alone. However, it should be kept in mind that the efficacy of dexamethasone in treating COVID-19 was proven in well-designed RCTs such as the RECOVERY study , whereas no such compelling RCTs have been performed for hydroxychloroquine.
3. What effect does a history of CVA have on COVID prognosis?
A)• In all the case series studied, history of stroke was associated with poorer progression of COVID-19. In a cohort of patients from 55 hospitals, history of stroke was twice as frequent among patients classified as having severe COVID-19 than among patients with mild symptoms. The virus enters the brain parenchyma, endothelium, and heart, and alters coagulation, which may lead to stroke
• The virus enters the brain parenchyma, endothelium, and heart, and alters coagulation, which may lead to stroke.
• History of stroke is associated with a three-fold increase in the risk of death due to SARS-CoV-2 infection
COVID CASE 21
Covid 19 with multiple comorbidities:
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-viral-pneumonia.html
1)What do you think are the factors in this patient that are contributing to his increased severity of symptoms and infection?
A)• Comorbidities like
• Diabetes mellitus since 7years
• Asthma since 7 years
• History of pulmonary kochs which might have caused some lung damage.
• History of pneumonia might have caused damage in lungs.
• Chronic kidney disease since 2yrs.
2)Can you explain why the D dimer levels are increasing in this patient?
A)• D dimer is a product after clot is degraded.
• In covid 19 infection,thrombotic events takes place due to release of clotting factors
3)What were the treatment options taken up with falling oxygen saturation?
A)• 15 litres of oxygen/minute was given
• Patient was intubated when oxygen saturation fell to 30%.
4) Can you think of an appropriate explanation as to why the patient has developed CKD, 2 years ago? (Note: Despite being on anti diabetic medication, there was no regular monitoring of blood sugar levels and hence no way to know for sure if it was being controlled or not)
MASTER CHART for covid cases:
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