OPINION OF CASES BY 172
NEUROLOGY
Case A:
A 40 year old male presented to the hospital from Yadagirigutta with the
chief complaints of irrelevant talking and decreased food intake since 9
days.
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.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:
12 YEARS AGO
·
Addicted to alcohol, drinks about 3-4 quarters per
day
2 YEARS AGO
·
Diagnosed with type 2 Diabetes (irregular
medication; once in 2 or 3 days)
1 YEAR AGO
·
1-2 episodes of seizures (mostly due to alcohol
consumption)
4 MONTHS AGO
·
Developed a seizure (mostly GTCS)
·
Cessation of alcohol for 24 hours assosiated with
symptoms of restlessness, sweating, and tremors.
10 DAYS AGO
·
General body pains
9 DAYS AGO
·
Started talking and laughing to himself (sudden
onset)
·
Decreased food intake
·
Required assistance to move around
·
Short term memory loss (couldn't recognise family
members)
·
ANATOMICAL LOCALISATION
PRIMARY ETIOLOGY
·
Wernicke's encephalopathy: thiamine deficiency
secondary to alcohol dependence
·
Uremic encephalopathy:
·
Altered sensorium: alcohol withdrawal syndrome
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
1) Drug name: SYP POTKLOR
MOA: It inceases the
potassium levels
Indication: This medicine is
used for the prevention or treatment of low potassium levels in the blood
(Hypokalemia).
2)Drug name: PREGABALIN
MOA: Although the
mechanism of action has not been fully elucidated, studies involving structurally
related drugs suggest that presynaptic binding of pregabalin to voltage-gated
calcium channels is key to the antiseizure and antinociceptive effects observed
in animal models.
Indication: Pregabalin is
indicated for the management of neuropathic pain associated with diabetic
peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain
associated with spinal cord injury, and as adjunctive therapy for the treatment
of partial-onset seizures
Efficacy over
Pregabalin:
·
P : 539
·
I : pregabalin
·
C : 265
·
O : the most common adverse events were
dizziness and somnolence
https://go.drugbank.com/drugs/DB00230
https://pubmed.ncbi.nlm.nih.gov/30242745/
3) Drug name: KCl
MOA: For use as an
electrolyte replenisher and in the treatment of hypokalemia.
Indication: For use as an
electrolyte replenisher and in the treatment of hypokalemia.
Efficacy over KCL:
·
p : 18
·
i : KCl
·
c : random number of patients
·
o : amiloride might be more
effective than potassium chloride in preventing hypokalaemia
https://go.drugbank.com/drugs/DB00761
https://pubmed.ncbi.nlm.nih.gov/3911735/
·
INJ NS and RL : Lactated Ringer's is
a sterile, nonpyrogenic solution for fluid and electrolyte replenishment
and caloric supply in a single dose container for intravenous administration.
https://www.rxlist.com/lactated-ringers-in-5-dextrose-drug.htm
4) Drug name: LORAZEPAM
MOA: Lorazepam
allosterically binds on the benzodiazepine receptors in the post-synaptic
GABA-A ligand-gated chloride channel in different sites of the central nervous
system (CNS). This binding will result in an increase on the GABA inhibitory
effects which is translated as an increase in the flow of chloride ions into
the cell causing hyperpolarization and stabilization of the cellular plasma
membrane.
Indication: Lorazepam is
FDA-approved for the short-term relief of anxiety symptoms related to anxiety
disorders and anxiety associated with depressive symptoms such as
anxiety-associated insomnia. It is as well used as an anesthesia premedication
in adults to relieve anxiety or to produce sedation/amnesia and for the
treatment of status epilepticus.
Efficacy over
lorazepam:
·
P : 56
·
I : lorazepam
·
C : 21
·
O : The effect size achieved in the placebo group
was not inferior to that of benzodiazepines in general.
https://go.drugbank.com/drugs/DB00186
https://pubmed.ncbi.nlm.nih.gov/2575766/
3) Why have
neurological symptoms appeared this time, that were absent during withdrawal
earlier? What could be a possible cause for this?
Patient had increased
symptoms because he relapsed and drank alcohol again. Usually if you stop
taking alcohol and start again patient will have severe withdrawal symtoms next
time whenn he stops.
4) What is the
reason for giving thiamine in this patient?
Wernicke’s
encephalopathy is an acute neuropsychiatric disorder that occurs as a result of
thiamine (vitamin B1) deficiency. Thiamine has been administered to
counteract its deficiency.
5) What is the
probable reason for kidney injury in this patient?
Chronic alcohol
consumption might have lead to kidney injury in this patient.
6). What is the
probable cause for the normocytic anemia?
The most common
cause of normocytic anemia is a long-term (chronic) disease. In this
case, the patient has been suffering from uremic encephalopathy which is
an organic brain disorder. It develops in patients with acute or chronic renal
failure, usually when the estimated glomerular filtration rate falls and
remains below 15 mL/min.
7) Could chronic
alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Yes, excessive
alcohol can cause nutritional deficiencies and alcohol toxicity. These in turn
can cause poor nutrition leading topoor wound healing and problems with nerves.
When the sensory nerves in the foot stop working, the foot can get injured and
this leads to food ulcers.
Case B:
A 52 year old male came to the hospital 2 days back presenting
with slurring of speech and deviation of mouth that
lasted for 1 day and resolved on the same day.
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
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
7 DAYS AGO
·
Giddiness assosiated with an episode of vomiting
3 DAYS AGO
·
Giddiness - sudden in onset
- continuous
and gradually progressive
-increased
in severity upon getting up from the bed and while walking
-associated with bilateral Hearing loss, aural fullness and presence of
tinnitus
·
Vomiting (2-3 episodes per day), non projectile,
non bilious containing food particles
·
Postural instability
ANATOMICAL LOCALISATION
ETIOLOGY OF DISEASE IN PATIENT
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
3) Did the patients
history of denovo HTN contribute to his current condition?
The patients history
of denovo HTN might have been contributed to his current condition as, long
history and irregular medication can lead to peripheral neuropathy which in
this case might have lead to cerebral atresia.
4) Does the
patients history of alcoholism make him more susceptible to ischaemic or
haemorrhagic type of stroke?
Alcohol may increase
the risk of hemorrhagic stroke. It is caused by a blood clot blocking the flow
of blood and oxygen from reaching the brain.
Case C:
A 45 years old female ,house wife by occupation came to opd with
chief complaints of palpitations, chest heaviness, pedal edema, chest pain,
radiating pain along her left upper limb.
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.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
10 YEARS AGO
·
Paralysis of both upper and lower limbs (right and
left)
1 YEAR AGO
·
Right and left paresis due to hypokalemia
8 MONTHS AGO
·
Bilateral pedal edema - gradually progressing
- present both in sitting and
standing position
- relieved on taking medication
·
Swelling over the legs (bilateral)
7 MONTHS AGO
·
Blood infection
2 MONTHS AGO
·
Treatment of neck pain
6 DAYS AGO
·
Pain - radiating along the the left upper
limb
- dragging in nature, aggrevated
during palpitations
- relieved by
taking medication for palpitations
·
Chest pain associated with chest heaviness
5 DAYS AGO
·
Could feel her own heartbeat
·
Chestpain
·
Difficulty in breathing
·
Palpitations - since sudden in onset, more during
night time
·
- aggregated by lifting weights, speaking
continuously
·
- it is
relieved by drinking more water and medication
·
Dyspnoea during palpitations (NHYA-CLASS-3)
ANATOMICAL LOCALISATION
·
Neural system due to hypokalemia
PRIMARY ETIOLOGY
·
Most probably due to the electrolyte imbalances.
2) What are the
reasons for recurrence of hypokalemia in her? Important risk factors for her
hypokalemia?
Reason for recurrence
of hypokalemia in this patient is due to recurrent hypokalemic periodic
paralysis. The current risk factor is mainly due to administration of
diuretics. Other risk factors are:
a) Abnormal loses due
to medications, osmotic diuresis, renal tubular acidosis, hypomagnesemia.
b) Trance cellular
shifts
c) Inadequate intake
d) Pseudohypokalemia
3) What are the
changes seen in ECG in case of hypokalemia and associated symptoms?
ECG changes include:
·
Flattening and inversion of T waves in mild
hypokalemia
·
Q-T interval prolongation
·
Visible U wave and mild ST depression in more
severe hypokalemia
·
Severe hypokalemia can also result in arrhythmias
such as Torsades de points and ventricular tachycardia.
Clinical symptoms of hypokalemia do not become evident until the serum
potassium level is less than 3 mmol/L. The severity of symptoms also tends to
be proportional to the degree and duration of hypokalemia.
The assosiated symptoms are:
·
Muscle weakness (the pattern is
ascending in nature affecting the lower extremities, progressing to involve the
trunk and upper extremities and potentially advancing to paralysis).
·
Fatigue
·
Constipation
·
Muscle twitches
·
Palpitations
In more severe
cases, abnormal rythms may occurs:
·
Atrial or ventricular fibrillation
·
Premature heartbeats
·
Tachycardia
·
Bradycardia
Case D:
A 55year old male patient came to OPD with c/o altered sensorium and
involuntary movements from 11pm and recurrent episodes of seizures since 5yrs.
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
Questions:
1) Is there
any relationship between occurrence of seizure to brain stroke. If yes what is
the mechanism behind it?
Yes, post‐stroke seizure and post‐stroke epilepsy are common causes of
hospital admissions, either as a presenting feature or as a complication after
a stroke. Also taking into consideration the age of our patient, it is to be noted
that stroke is the most common cause of seizures in the elderly population.
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
·
Hyperperfusion injury.
Late onset seizures are associated with the persistent changes in
neuronal excitability and gliotic scarring. Haemosiderin deposits are
thought to cause irritability after a haemorrhagic stroke.
2) In the previous
episodes of seizures, patient didn't loose his consciousness but in the recent
episode he lost his consciousness what might be the reason?
The patient might
have experienced a grand mal seizure — also known as a generalized
tonic-clonic seizure in his last episode. It is defined as a
seizure that has a tonic phase followed by clonic muscle
contractions. They are usually associated with impaired awareness or
complete loss of consciousness.
Case E:
A 48-year-old gentleman hailing from
a small town in Telangana presented to the casualty ward on 25th April 2021 at
7:40am with the chief complaints of unresponsiveness for 7 hours and 3
intermittent episodes of seizures in the past 3 hours.
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Questions:
1) What could have
been the reason for this patient to develop ataxia in the past 1 year?
Ataxia usually
results from damage to a part of the brain called the cerebellum, but it can
also be caused by damage to other parts of the nervous system.
This damage can be
caused by
·
a head injury
·
lack of oxygen
·
long-term consumption of alcohol.
·
underlying conditions such as MS
As the patient
has a h/o minor head injuries and addiction to alcohol since 3 years, he
might've developed ataxia.
2) What was the
reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?
The probable reasons
for IC bleed in this case are:
·
Chronic alcohol abuse assosiated to high blood
pressure which can cause the thin-walled arteries which supply blood to the
brain to rupture, releasing blood into the brain tissue.
·
Untreated head injuries
Assosiation of
alcohol with bleeding disorders:
·
Alcohol has numerous adverse effects on the various
types of blood cells and their functions. Heavy alcohol consumption can cause
generalized suppression of blood cell production and the production of structurally
abnormal blood cell precursors that cannot mature into functional cells.
·
Alcoholics frequently have defective red
blood cells that are destroyed prematurely, possibly resulting in anemia.
·
Alcohol also interferes with the production and
function of white blood cells, especially those that defend the body against
invading bacteria.
·
Consequently, alcoholics frequently suffer
from bacterial infections. Finally, alcohol adversely affects the platelets and
other components of the blood-clotting system. Heavy alcohol consumption thus
may increase the drinker's risk of suffering a stroke.
Case F:
A 30 year old male patient
lorry driver by occupation came to the OPD with chief complaints of weakness of
right upper and lower limb since one day and deviation of mouth towards left
since one day.
Questions:
1. Does the patient's history of road traffic accident have any
role in his present condition?
No.
2. What are warning signs of CVA?
·
Sudden numbness or weakness in the
face, arm, or leg, especially on one side of the body.
·
Sudden confusion, trouble speaking, or
difficulty understanding speech.
·
Sudden trouble seeing in one or
both eyes.
·
Sudden trouble walking, dizziness, loss
of balance, or lack of coordination.
·
Sudden severe headache with no
known cause.
3.What is the drug
rationale in CVA?
·
Drug treatment of CVA involves intravenous
thrombolysis with alteplase. Intravenous alteplase promotes thrombolysis by
hydrolyzing plasminogen to form the proteolytic enzyme plasmin. Plasmin targets
the blood clot with limited systemic thrombolytic effects.
·
Other acute supportive interventions for CVA
include maintaining normoglycemia, euthermia and treating severe
hypertension.
·
Urgent antiplatelet use for AIS has limited
benefits and should only promptly be initiated if alteplase was not
administered, or after 24 hours if alteplase was administered.
4. Does alcohol has
any role in his attack?
Liver damage in
chronic alcoholics can stop the liver from making substances that help
blood to clot. This can increase your risk of having a stroke caused
by bleeding in your brain.
5.Does his lipid
profile has any role for his attack?
No.
Case G:
50-year-old male patient presented to hospital with complaints of
weakness of all four limbs since 8 PM yesterday.
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
Questions:
1) What is
myelopathy hand ?
A characteristic
dysfunction of the hand in cervical spinal disorders with 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. It appears to be
due to pyramidal tract involvement.
2) What is finger
escape ?
It
refers to the slightly greater abduction of the fifth digit, due to paralysis
of the abducting palmar interosseous muscle and unopposed action of the radial
innervated extensor muscles.
3) What is
Hoffman’s reflex?
Hoffmann's
reflex is a neurological examination finding elicited by a reflex
test which can help verify the presence or absence of issues arising from
the corticospinal tract.
Case H:
A 17 year old
female student by occupation presented to causality on 1/5/2021 with chief
complaints of involuntary movements of both upper and lower limbs a day
before.
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Questions:
1) What can be
the cause of her condition ?
2) What are the
risk factors for cortical vein thrombosis?
·
·
Risk factors for children and infants include:
·
Beta-thalassemia major
·
Heart disease — either congenital (you're born with
it) or acquired (you develop it)
·
Iron deficiency
·
Certain infections
·
Dehydration
·
Head injury
·
Sickle cell anemia
·
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
·
Collagen vascular diseases
·
Obesity
·
Cancer
·
Inflammatory bowel disease like Crohn's
·
Low blood pressure in the brain
·
3)There was seizure
free period in between but again sudden episode of GTCS, why? Resolved
spontaneously, why?
3 days after seizure
free period patient was tapered off Midazolam, phenobarbitone. ThIs might
be the cause of GTCS.
4) What drug was
used in suspicion of cortical venous sinus thrombosis?
Clexane 0.4ml/sc was
started in suspicion of CSVT
GASTROENTROLOGY
Case A:
A 33 yr old male daily wage labour worker from miryalaguda who is a
chronic alcoholic and smoker came to hospital on 30/04/2021 with cheif
complaints with of pain abdomen & vomiting since 1 week and constipation,
burning micturition, fever since 4 days.
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.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
5 YEARS AGO
·
Pain in abdomen
·
Vomiting
(subsided by
conservatibe treatment and abstinence of alcohol)
ONE YEAR AGO
·
Pain in abdomen and vomiting: 5-6 episodes
(resumed frequent
intake of alcohol; conservative treatment by local RMP)
ONE WEEK AGO
·
Abdominal pain- 1) in umbilical, left hypochondriac,
left lumbar and hypogastric region
2) throbbing type and radiating to
back
3) assosiated with nausea and
vomiting
·
Vomiting (one episode) - non bilious, non
projectile, contains food particles and water
4 DAYS AGO
·
Fever
·
Constipation
·
Burning micturition
DURING HOSPITAL STAY
·
Developed progressive pneumothorax
ANATOMICAL LOCALISATION
1. PANCREAS- a) Acute on
chronic pancreatitis
b) Acute infective peri pancreatic fluid collections
2. LESSER SAC- a)
Pseudocyst
3. LEFT LUNG- a)
Moderate left pleural effusion with basal atelectasis
ETIOLOGY OF DISEASE IN PATIENT
·
The main cause of pancreatitis in this patient is
attributed to the chronic intake of alcohol.
·
Recurrent episodes of pancreatitis has to lead to
various complications of pseudocyst formation in lesser sac due to pancreatic
duct rupture and BRONCHO PLEURAL FISTULA leading to pneumothorax.
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?
Octreotide:
The results of
clinical investigations using somatostatin or its analogue are controversial,
since all these trials had low statistical power. In a recent multicenter
randomized controlled study with a large number of patients, no benefit of
octreotide on progression or outcome was found. Chronic pancreatitis is
characterized by an irreversible destruction of the exocrine and endocrine
pancreatic parenchyma leading to maldigestion and diabetes. Pain, which may be
caused by increased ductal pressure, is one of the most dominant symptoms in
chronic pancreatitis. However, no beneficial effects on pain with pancreatic
exocrine secretion-inhibiting drugs have been demonstrated. Treatment of other
complications of the disease (pseudocyst formation, fistula and pancreatic
ascites), with somatostatin or octreotide has given conflicting results.
However, in a prophylactic clinical setting (e.g. elective pancreatic surgery)
the inhibition of exocrine pancreatic secretion reduces complications.
A clinical and
therapeutical study of 47 patients with the diagnosis of acute pancreatitis is
reported. According to Ranson's criteria patients were initially classified as
suffering from mild (28) and severe (18) acute pancreatitis. Twenty-eight, 11,
7 and 1 patients had biliary, alcoholic, idiopathic and neoplastic causes,
respectively, of their conditions. The classification of episodes was made on
the basis of clinical manifestations, biologic investigations, and imaging diagnosis,
and is shown in the corresponding tables. The therapeutic profile was a
randomized double-blind study: perfused somatostatin (SS) versus placebo (P)
(physiologic saline 0.9%). The administration of somatostatin in perfusion (250
mcg/h/48 hours) did not improve significantly the parameters used to score the
severity, although the mortality rate decreased significantly (p < 0.05) in
the group of patients with the severe form of the disease.
Antibiotics:
The mortality rates
were 5.26% (5/95) and 18.18% (16/88) in prophylactic antibiotics and
placebo/none-treatment groups, respectively.
Material and methods:
Seventy-three patients with severe pancreatitis were included in a prospective,
randomized, clinical study in seven Norwegian hospitals. The number of patients
was limited to 73 because of slow patient accrual. Severe pancreatitis was
defined as a C-reactive protein (CRP) level of >120 mg/l after 24 h or CRP
>200 48 h after the start of symptoms. The patients were randomized to
either early antibiotic treatment (imipenem 0.5 g x 3 for 5-7 days) (imipenem
group) (n=36) or no antibiotics (control group) (n=37).
Results: The groups
were similar in age, cause of pancreatitis, duration of symptoms and APACHE II
score. Patients in the imipenem group experienced lower rates of complications
(12 versus 22 patients) (p=0.035) and infections (5 versus 16 patients)
(p=0.009) than those in the control group. There was no difference in length of
hospital stay (18 versus 22 days), need of intensive care (8 versus 7 patients),
need of acute interventions (10 versus 13), nor for surgery (3 versus 3) or
30-day mortality rates (3 versus 4).
Conclusions: The
study, although underpowered, supports the use of early prophylactic treatment
with imipenem in order to
https://pubmed.ncbi.nlm.nih.gov/17506001/
TPN
The aim of the study
was to evaluate and control the therapeutic validity of Somatostatin
administration and the clinical benefits of parenteral nutrition during acute
pancreatitis. We selected 31 patients with 1st and 2nd degree pancreatitis
according to Ranson's classification. Diagnosis was based on clinical and
humoral data and confirmed by echography and CT examinations. The most common
etiological cause was biliary++ lithiasis (74.2%). All the patients in the
study were split into two groups and received conventional treatment. The
therapeutic schedule administered to group 1 included somatostatin (250
micrograms/h for 72-96 h), while group 2 received total parenteral nutrition
with 2,000-2,500 Kal/day trough a central vein. The data obtained from our study
demonstrated that both somatostatin and parenteral nutrition are valid tools
during the acute phase of the disease. It must be pointed out that the former
significantly influences the clinical course and allows a precise control of
the painful symptomatology, the objective picture and the curve of the main
hematochemical parameters. Parenteral nutrition betters the anabolic response
of the organism during the acute phase and carries out an indirect
antienzymatic response, so favouring a quicker recovery than observed in the
group treated with somatostatin.
https://pubmed.ncbi.nlm.nih.gov/2566958/
USG drain
A single-center
retrospective study was performed after obtaining Institutional review board
approval for analyzing hospital records of patients with acute necrotizing
pancreatitis from January 2012 to July 2017. Seventy-eight consecutive patients
with necrotizing pancreatitis and acute necrotic collections (ANC) were managed
with percutaneous catheter drainage (PCD) and catheter-directed necrosectomy,
in early phase of the disease (< 21 days). Clinical data and laboratory
parameters of the included patients were evaluated until discharge from
hospital, or mortality.
Results
Overall survival rate
was 73.1%. Forty-two (53.8%) patients survived with PCD alone, while the
remaining 15 (19.2%) survivors needed additional necrosectomy. The timing of
intervention from the start of the hospitalization to drainage was 14.3 ± 2.4
days. Significant risk factors for mortality were the presence of organ system
failure, need for mechanical ventilation, renal replacement therapy, and the
acute physiology and chronic health evaluation II (APACHE II) score. An APACHE
II score cutoff value of 15 was a significant discriminant for predicting
survival with catheter-directed necrosectomy.
Conclusion
An early PCD of ANC
in clinically deteriorating patients with acute necrotizing pancreatitis, along
with aggressive catheter-directed necrosectomy can avoid surgical
interventions, and improve outcome in a significant proportion of patients with
acute necrotizing pancreatitis.
https://link.springer.com/article/10.1007/s12664-019-00969-0
Case B:
Case of 52 year old man with severe epigastric pain.
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
Questions:
1) What is causing
the patient's dyspnea? How is it related to pancreatitis?
In the pathogenesis
of respiratory complications of pancreatitis, inflammatory mediators released
from pancreatic injury and digestive actions of pancreatic enzymes play a key
role. The role of active digestive enzymes in circulation, release of multiple
pro-inflammatory cytokines, activation and migration of leukocytes/neutrophils,
complement mediated injury, and platelet activating factors are primarily
involved in development of these complication. A damage to the pulmonary
vasculature caused by activated trypsin leads to increased endothelial
permeability while the main culprit for pulmonary complications.
2) Name possible
reasons why the patient has developed a state of hyperglycemia.
β-cell function
inversely regulates α-cell function via paracrine mechanisms within the islet,
the initial defects in insulin secretion seen in chronic pancreatitis are
associated with increases in glucagon secretion that may contribute to early
impairment in glucose tolerance, and correlates with an increase in the numbers
of islet α-cells observed pathologically. However, with progressive islet
damage during the course of T3cDM diabetes, glucagon secretion becomes
impaired, which may contribute to the development of brittle diabetes late in
the disease.
3) What is the
reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty
Liver disease?
According to the
report the patient has grade I fatty livver due to his chronic consumption of
alcohol which might've caused elevated LFT's.
The biochemical
markers for chronic alcohol consumption that have been most commonly studied
are serum GGT, AST, ALT, mean corpuscular volume (MCV) and
carbohydrate-deficient transferrin (CDT). An AST to ALT ratio over 2 is highly
suggestive of ALD. Most patients with non-ALD have AST to ALT ratios below one.
Specific IgA antibodies directed towards acetaldehyde-derived protein
modifications are frequently seen alcoholics and thus IgA levels are increased
in chronic ALD. An increased ratio of IgA to IgG is highly suggestive of ALD.
Chronic alcohol
consumption is known to induce a rise in serum GGT and is a widely used index
for excessive alcohol use. However, elevated GGT alone has both low
sensitivity and specificity for alcohol abuse. GGT is not specific to
alcoholism and is increased in many conditions such as obesity, advanced age,
moderate alcohol consumption, all forms of liver disease including fatty liver
and in particular intra and extrahepatic biliary obstruction, hepatocellular
carcinoma and phenytoin use. The sensitivity of GGT as a marker for alcohol
consumption in young adults has been showed to be particularly poor even in
cases of documented alcohol dependence.
4) What is the line
of treatment in this patient?
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 C:
A 45 year old Female patient, came to Hospital with cheif complaints of:
·
Fever
since 3 days
·
Pain in
abdomen since 2 days
·
Decreased
urine output since 2 days
·
Abdominal
distention since morning
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Questions:
1) What is the most
probable diagnosis in this patient?
The probable
diagnosis in this case is Analgesic Nephropathy.
2) What was the
cause of her death?
The cause of death in
this may be due to sepsis.
3) Does her NSAID
abuse have something to do with her condition? How?
As the patient has
Grade III RPD changes in her right kidney she may have an underlying CKD which
is secondary to her NSAID abuse.
NEPHROLOGY
Case A:
A 52 yr
old male patient who is a farmer by occupation presented to hospital on 17 May
2021 with chief complaints of SOB since 4 days, burning micturition
since 4 days and fever since 2 days.
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
Questions:
1. What could be
the reason for his SOB ?
Chronic kidney
disease can lead to anemia which leaves the blood short of red blood cells with
which to carry oxygen. Anemia and the need to be more active can lead to our
body struggling to get enough oxygen for our muscles and can leave us out of
breath.
Kidney disease is
one of the more common complications of diabetes, affecting about 40% of people
with diabetes.
2. Why does he have
intermittent episodes of drowsiness ?
A case of slight/mild
hyponatremia may cause fatigue, restlessness, confusion and sluggishness.
Drowsiness in this patient may be due to hyponatremia because patient
showed improvement after administration of sodium.
3. Why did he
complain of fleshy mass like passage in his urine?
Fleshy mass like
passage in urine is due to pyuria. Pus cells in the urine appear as fleshy
mass.
4. What are the
complications of TURP that he may have had?
He seems to face
electrolyte imbalance post TURP.
Case B:
An 8 year old with frequent urination.
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 ?
The child seems to be
psycho somatic, hence the behaviour.
2. Why doesn't the
child have the excessive urge of urination at night time ?
The child has
excessive urge to urinate during the daytime even though the bladder isn't full
because of his psychological impulse to urinate. During the night time he
wouldn't have the compulsion to do so since he's asleep.
3. How would you
want to manage the patient to relieve him of his symptoms?
I wouldn't recommend
any medicines as such because all the reports, clinical findings seem normal.
He could be counselled mentally and go to therapy to overcome his psychological
compulsion to urinate excessive amount of times even when he doesn't need to. A
placebo might be of help.
INFECTIOUS DISEASES
Case A:
A 40 year old lady who works in cotton fields came to the hospital with
the chief complaints of difficulty in swallowing, fever and cough since 2
months.
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?
Characteristic
clinical history of tracheoesophageal fistula are :
·
cough
·
difficulty in swallowing
·
loss of weight
·
shortness of breath
Characteristic
physical findings of tracheoesophageal fistula are:
·
Fistulous communication between left
main bronchus and mid thoracic oesophagus.
2) What are the
chances of this patient developing immune reconstitution inflammatory syndrome?
Can we prevent it?
As patient is TB
positive, during or after completion of anti-TB therapy, there is a chance of
developing tuberculosis immune reconstitution inflammatory syndrome.
The most effective
prevention of immune reconstitution inflammatory syndrome would
involve initiation of ART before the development of advanced immunosuppression.
https://www.sciencedirect.com/science/article/pii/S2405579415300097
INFECTIOUS DISEASE AND HEPATOLOGY
Case A:
A 55 year old male patient who is a palm tree climber by occupation came
on 17th April 2021 with the chief complaints of pain in abdomen since
one week, decrease appetite since one week, fever since 2 days.
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
Questions:
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 ?
As mentioned patient
is chronic alcoholic and smoker. In 50% of the liver abscess cases these are
the predisposing factors.
2. What is the
etiopathogenesis of liver abscess in a chronic alcoholic patient ? (
since 30 years - 1 bottle per day)
3. Is liver abscess
more common in right lobe ?
50% of solitary liver
abscesses occur in the right lobe of the liver (a more significant part with
more blood supply), less commonly in the left liver lobe or caudate lobe.
4.What are the
indications for ultrasound guided aspiration of liver abscess ?
Indications
· Complicated diverticular abscess.
· Crohn's disease
related abscess.
· Complicated
appendicitis with appendicular abscess.
· Tuboovarian abscess.
· Post-surgical fluid
collections.
· Renal abscess or
retroperitoneal abscess.
·
Rplenic abscess.
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 B:
A 21 yr old male student, resident of nakrekal, came to the hospital
with chief complaints of abdominal pain since 20 days and fever since 18
days.
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
Questions:
1) Cause of liver
abcess in this patient ?
Infection
2) How do you
approach this patient ?
Antibiotics
3) Why do we treat
here ; both amoebic and pyogenic liver abcess?
If we dont treate
amobic liver abcess there is a chance that one of the following occurs:
·
a) Intraperitoneal, intrathoracic, or
intrapericardial rupture, with or without secondary bacterial infection.
· b) Extension to
pleura or pericardium.
· c) Dissemination
and formation of brain abscess.
·
· If we dont treate
pyogenic liver abcess there is a chance that one of the following occurs:
·
· a) Sepsis.
· b) Empyema
resulting from contiguous spread or intrapleural rupture of abscess.
· c) Rupture of abscess with
resulting peritonitis.
· d) Endophthalmitis
when an abscess is associated with K pneumoniae bacteremia.
4) Is there a way
to confirm the definitive diagnosis in this patient?
HEPATOLOGY
CASE A
A 55 year old male patient who is a palm tree
climber by Occupation
came on 17th April 2021 with the chief
Complaints of
PAIN ABDOMEN SINCE ONE WEEK
DECREASE APPETITE SINCE ONE WEEK
FEVER SINCE 2 DAYS
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 ?
As mentioned patient is chronic alcoholic and
smoker. In 50% of the liver abcess cases these ae the predisposing factors.
2. What is the etiopathogenesis of liver
abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
3. Is liver abscess more common in right lobe ?
50% of solitary liver abscesses occur in the right
lobe of the liver (a more significant part with more blood supply), less
commonly in the left liver lobe or caudate lobe.
4.What are the indications for ultrasound guided
aspiration of liver abscess?
Indications
- complicated diverticular abscess.
- Crohn's disease related abscess.
- complicated appendicitis with appendicular abscess.
- tuboovarian abscess.
- post-surgical fluid collections.
- hepatic abscess (e.g.
amoebic or post-operative)
- renal abscess or retroperitoneal abscess.
- splenic abscess.
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 B
CASE DISCUSSION
ON LIVER ABCESS
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
1) Cause of liver abcess in this patient ?
2) How do you approach this patient ?
3) Why do we treat here ; both amoebic and pyogenic
liver abcess?
- If we dont treate amobic liver abcess there is a chance that one of
the following occurs:
- Intraperitoneal, intrathoracic, or intrapericardial rupture, with
or without secondary bacterial infection.
- Direct extension to pleura or pericardium.
- Dissemination and formation of brain abscess.
- If we dont treate pyogenic liver abcess there is a chance that one
of the following occurs:
- Sepsis.
- Empyema resulting from contiguous spread or intrapleural rupture
of abscess.
- Rupture of abscess with resulting peritonitis.
- Endophthalmitis when an abscess is associated with
K pneumoniae bacteremia.
4) Is there a way to confirm the definitive
diagnosis in this patient?
PULMONOLOGY
CASE A
A 55 year old female patient, a
resident of Miryalaguda and farmer by occupation came to the hospital on
17/5/21 with the chief complaints of shortness of breath, pedal
edema and facial puffiness.
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 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
20 years ago:
Shortness of breath : on of off while working at
paddy field
relieved upon taking medication
12 years ago:
Episode of SOB : This one lasted 20 days and she
had to be hospitalized. The
SOB decreased upon treatment at the hospital.(grade II)
8 years ago
Similar
episodes of SOB every year each lasting approximately 1 week. Relieved upon taking
medication
Diabetes diagnosed
Polyuria
5 years ago:
Anemia treatment with iron injections
30 days back
Episode of SOB : insidious in onset and
gradual in progression.
occurred on exertion and
was relieved upon rest.
Generalised weakness
20 days back:
HRCT
outside which showed bronchiectasis
Hyperstension diagnosed
15 days back:
Pedal edema : upto the level ankle
pitting type.
Facial puffiness
2 days back:
SOB :even at rest (grade IV)
not relieved with
nebulizers
Drowsiness
Anatomical localization
Chronic obstructive pulmonary syndrome
Bronchiectasis
primary etiology
COPD is caused by prolonged
exposure to harmful particles or gases which may include second-hand
smoke, environmental and occupational exposures, and alpha-1 antitrypsin
deficiency. In this case patiemt is exposed to paddy frequently.
2) What are mechanism of action, indication and
efficacy over placebo of each of the pharmacological and non pharmacological
interventions used for this patient?
3) What could be the causes for her current acute
exacerbation?
Exacerbations of COPD are thought to be caused by
complex interactions between the host, bacteria, viruses, and environmental
pollution. These factors increase the inflammatory burden in the lower airways,
overwhelming the protective anti‐inflammatory defences leading to tissue
damage.
In this case, patient developed episodes commonly
around January, while working in paddy field. dust particles in the paddy
field or paddy can be the allergen that is causing the episodes.
4. Could the ATT have affected her symptoms? If so
how?
Patient has barrel shaped chest. Usually
barrel shaped chest is seen in emphysema. In emphysema there is ATT
deficiency. So deficiency of ATT could have affected her symptoms.
5.What could be the causes for her electrolyte
imbalance?
Serum electrolyte imbalance such as hyponatremia,
hypokalemia, hyperbilirubinemia, and elevated levels of transaminases, blood
urea, and serum creatinine are either caused by the disease process or the
therapy initiated
On Sat, May 29,
2021 at 3:02 PM 183 Sai Shreya Surapaneni <saishreya123@gmail.com> wrote:
NEUROLOGY
Case A:
A 40 year old male presented to the hospital from Yadagirigutta with the
chief complaints of irrelevant talking and decreased food intake since 9
days.
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.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:
12 YEARS AGO
·
Addicted to alcohol, drinks about 3-4 quarters per
day
2 YEARS AGO
·
Diagnosed with type 2 Diabetes (irregular
medication; once in 2 or 3 days)
1 YEAR AGO
·
1-2 episodes of seizures (mostly due to alcohol
consumption)
4 MONTHS AGO
·
Developed a seizure (mostly GTCS)
·
Cessation of alcohol for 24 hours assosiated with
symptoms of restlessness, sweating, and tremors.
10 DAYS AGO
·
General body pains
9 DAYS AGO
·
Started talking and laughing to himself (sudden
onset)
·
Decreased food intake
·
Required assistance to move around
·
Short term memory loss (couldn't recognise family
members)
ANATOMICAL LOCALISATION
PRIMARY ETIOLOGY
·
Wernicke's encephalopathy: thiamine deficiency
secondary to alcohol dependence
·
Uremic encephalopathy:
·
Altered sensorium: alcohol withdrawal
syndrome
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
3) Why have
neurological symptoms appeared this time, that were absent during withdrawal
earlier? What could be a possible cause for this?
4) What is the
reason for giving thiamine in this patient?
Wernicke’s
encephalopathy is an acute neuropsychiatric disorder that occurs as a result of
thiamine (vitamin B1) deficiency. Thiamine has been administered to
counteract its deficiency.
5) What is the
probable reason for kidney injury in this patient?
Chronic alcohol
consumption might have lead to kidney injury in this patient.
6). What is the
probable cause for the normocytic anemia?
The most common
cause of normocytic anemia is a long-term (chronic) disease. In this
case, the patient has been suffering from uremic encephalopathy which is
an organic brain disorder. It develops in patients with acute or chronic renal
failure, usually when the estimated glomerular filtration rate falls and
remains below 15 mL/min.
7) Could chronic
alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Case B:
A 52 year old male came to the hospital 2 days back presenting
with slurring of speech and deviation of mouth that
lasted for 1 day and resolved on the same day.
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
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?
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
3) Did the patients
history of denovo HTN contribute to his current condition?
4) Does the
patients history of alcoholism make him more susceptible to ischaemic or
haemorrhagic type of stroke?
Case C:
A 45 years old female ,house wife by occupation came to opd with
chief complaints of palpitations, chest heaviness, pedal edema, chest pain,
radiating pain along her left upper limb.
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.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?
2) What are the
reasons for recurrence of hypokalemia in her? Important risk factors for her
hypokalemia?
3) What are the
changes seen in ECG in case of hypokalemia and associated symptoms?
ECG changes include:
·
Flattening and inversion of T waves in mild
hypokalemia
·
Q-T interval prolongation
·
Visible U wave and mild ST depression in more
severe hypokalemia
·
Severe hypokalemia can also result in arrhythmias
such as Torsades de points and ventricular tachycardia.
Clinical symptoms of hypokalemia do not become evident until the serum
potassium level is less than 3 mmol/L. The severity of symptoms also tends to
be proportional to the degree and duration of hypokalemia.
The assosiated symptoms are:
·
Muscle weakness (the pattern is
ascending in nature affecting the lower extremities, progressing to involve the
trunk and upper extremities and potentially advancing to paralysis).
·
Fatigue
·
Constipation
·
Muscle twitches
·
Palpitations
In more severe
cases, abnormal rythms may occurs:
·
Atrial or ventricular fibrillation
·
Premature heartbeats
·
Tachycardia
·
Bradycardia
Case D:
A 55year old male patient came to OPD with c/o altered sensorium and
involuntary movements from 11pm and recurrent episodes of seizures since 5yrs.
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
Questions:
1) Is there
any relationship between occurrence of seizure to brain stroke. If yes what is
the mechanism behind it?
Yes, post‐stroke seizure and post‐stroke epilepsy are common causes of
hospital admissions, either as a presenting feature or as a complication after
a stroke. Also taking into consideration the age of our patient, it is to be
noted that stroke is the most common cause of seizures in the elderly
population.
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
·
Hyperperfusion injury.
Late onset seizures are associated with the persistent changes in
neuronal excitability and gliotic scarring. Haemosiderin deposits are
thought to cause irritability after a haemorrhagic stroke.
2) In the previous
episodes of seizures, patient didn't loose his consciousness but in the recent
episode he lost his consciousness what might be the reason?
The patient might
have experienced a grand mal seizure — also known as a generalized
tonic-clonic seizure in his last episode. It is defined as a
seizure that has a tonic phase followed by clonic muscle
contractions. They are usually associated with impaired awareness or
complete loss of consciousness.
Case E:
A
48-year-old gentleman hailing from a small town in Telangana presented to the
casualty ward on 25th April 2021 at 7:40am with the chief complaints of
unresponsiveness for 7 hours and 3 intermittent episodes of seizures in the
past 3 hours.
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Questions:
1) What could have
been the reason for this patient to develop ataxia in the past 1 year?
Ataxia usually
results from damage to a part of the brain called the cerebellum, but it can
also be caused by damage to other parts of the nervous system.
This damage can be
caused by
·
a head injury
·
lack of oxygen
·
long-term consumption of alcohol.
·
underlying conditions such as MS
As the patient
has a h/o minor head injuries and addiction to alcohol since 3 years, he
might've developed ataxia.
2) What was the
reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?
The probable reasons
for IC bleed in this case are:
·
Chronic alcohol abuse assosiated to high blood
pressure which can cause the thin-walled arteries which supply blood to the
brain to rupture, releasing blood into the brain tissue.
·
Untreated head injuries
Assosiation of
alcohol with bleeding disorders:
·
Alcohol has numerous adverse effects on the various
types of blood cells and their functions. Heavy alcohol consumption can cause
generalized suppression of blood cell production and the production of
structurally abnormal blood cell precursors that cannot mature into functional
cells.
·
Alcoholics frequently have defective red blood
cells that are destroyed prematurely, possibly resulting in anemia.
·
Alcohol also interferes with the production and
function of white blood cells, especially those that defend the body against
invading bacteria.
·
Consequently, alcoholics frequently suffer
from bacterial infections. Finally, alcohol adversely affects the platelets and
other components of the blood-clotting system. Heavy alcohol consumption thus
may increase the drinker's risk of suffering a stroke.
Case F:
A 30 year
old male patient lorry driver by occupation came to the OPD with chief
complaints of weakness of right upper and lower limb since one day and
deviation of mouth towards left since one day.
Questions:
1. Does the patient's history of road traffic
accident have any role in his present condition?
No.
2. What are warning signs of CVA?
·
Sudden numbness or weakness in the
face, arm, or leg, especially on one side of the body.
·
Sudden confusion, trouble speaking, or
difficulty understanding speech.
·
Sudden trouble seeing in one or
both eyes.
·
Sudden trouble walking, dizziness, loss
of balance, or lack of coordination.
·
Sudden severe headache with no
known cause.
3.What is the drug
rationale in CVA?
·
Drug treatment of CVA involves intravenous
thrombolysis with alteplase. Intravenous alteplase promotes thrombolysis by
hydrolyzing plasminogen to form the proteolytic enzyme plasmin. Plasmin targets
the blood clot with limited systemic thrombolytic effects.
·
Other acute supportive interventions for CVA
include maintaining normoglycemia, euthermia and treating severe
hypertension.
·
Urgent antiplatelet use for AIS has limited
benefits and should only promptly be initiated if alteplase was not
administered, or after 24 hours if alteplase was administered.
4. Does alcohol has
any role in his attack?
Liver damage in
chronic alcoholics can stop the liver from making substances that help
blood to clot. This can increase your risk of having a stroke caused
by bleeding in your brain.
5.Does his lipid
profile has any role for his attack?
No.
Case G:
50-year-old male patient presented to hospital with complaints of
weakness of all four limbs since 8 PM yesterday.
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
Questions:
1) What is
myelopathy hand ?
A characteristic
dysfunction of the hand in cervical spinal disorders with 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. It appears to be
due to pyramidal tract involvement.
2) What is finger
escape ?
It
refers to the slightly greater abduction of the fifth digit, due to paralysis
of the abducting palmar interosseous muscle and unopposed action of the radial
innervated extensor muscles.
3) What is Hoffman’s
reflex?
Hoffmann's
reflex is a neurological examination finding elicited by a reflex
test which can help verify the presence or absence of issues arising from
the corticospinal tract.
Case H:
A 17 year old
female student by occupation presented to causality on 1/5/2021 with chief
complaints of involuntary movements of both upper and lower limbs a day
before.
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Questions:
1) What can be
the cause of her condition ?
2) What are the
risk factors for cortical vein thrombosis?
·
·
Risk factors for children and infants include:
·
Beta-thalassemia major
·
Heart disease — either congenital (you're born with
it) or acquired (you develop it)
·
Iron deficiency
·
Certain infections
·
Dehydration
·
Head injury
·
Sickle cell anemia
·
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
·
Collagen vascular diseases
·
Obesity
·
Cancer
·
Inflammatory bowel disease like Crohn's
·
Low blood pressure in the brain
·
3)There was seizure
free period in between but again sudden episode of GTCS, why? Resolved
spontaneously, why?
4) What drug was
used in suspicion of cortical venous sinus thrombosis?
CARDIOLOGY
Case A:
A 78 yr old male patient, resident of of kattangur and
shepherd by occupation came to the OPD on 14 /5/2021 with chief
complaints of:
·
shortness
of breath, since 20 days
·
chest
pain, since 20 days
·
B/L pedal
edema, since 4 days
·
facial
puffiness, since 4 days
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.
Questions:
1.What is the
difference between heart failure with preserved ejection fraction and with
reduced ejection fraction?
2.Why haven't we
done pericardiocenetis in this pateint?
Pericardiocentesis is
a procedure done to remove fluid that has built up in the sac around the pericardium. In
this case, to keep a check if patient is having cardiac tamponade , review of
ECHO has been done. As no cardiac tamponade was seen this procedure wasn't
performed.
3.What are the risk
factors for development of heart failure in the patient?
The risk factors of
heart failure are:
·
Hypertension
·
Coronary artery disease
·
Diabetes
·
Certain medication
·
Alcohol abuse
·
Smoking
·
Obesity
·
Congenital heart defects
·
Sleep apnea
4.What could be the
cause for hypotension in this case?
The patient is suffering
from acute, rapid accumulation of fluid in the pericardium which causes signs
of acute hemodynamic compromise in cardiac tamponade. Patients with this
condition develop tachycardia, hypotension and distended neck veins.
Case B:
A 73 yr male patient teacher by occupation, presented to OPD with
chief complaints of :
·
Pedal
edema, since 15 days
·
Shortness
of breath, since 4 days
·
Decreased
urine output, since 2 days
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html.
Questions:
1.What are the
possible causes for heart failure in this patient?
The probable causes
for heart failure in this patient are:
·
Chronic alcohol abuse
·
Long standing case of hypertension (19 years)
·
Stage 4 Chronic Kidney disease
2. What is the
reason for anaemia in this case?
3.What is the
reason for blebs and non healing ulcer in the legs of this patient?
Leg and foot ulcers
in diabetic patients have three common underlying causes: venous insufficiency,
peripheral neuropathy, or peripheral arterial occlusive disease.
4. What sequence of
stages of diabetes has been noted in this patient?
Case C:
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.
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.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
10 YEARS AGO
·
Surgery for inguinal hernia
3 YEARS AGO
·
Aggravated on and off pain at the site of surgery
·
On and off facial puffiness
1 YEAR AGO
·
Grade II shortness of breath - diagnosed for HTN
(on medication)
2 DAYS AGO
·
Shortness of breath Grade II (on exertion)
·
Decreased urine output
·
Constipation
ONE DAY AGO
·
Shortness of breath Grade IV (at rest)
DAY OF ADMISSION
·
Anuria
ANATOMICAL LOCALISATION
1. HEART: a) Atrial
fibrillation with Rapid ventricular response
b) Thrombi noted in Left Atrial Appendages and Left atrium
c) Dilated Main Pulmonary Artery and Left Pulmonary Arteries
d) Severe LV dysfunction
e) IVC dilated
2. KIDNEY: a) Cardiorenal syndrome
ETIOLOGY OF DISEASE IN PATIENT
·
Loss of Atrial contraction and Left atrial
dilatation causes stasis of blood in the LA and may lead to thrombus formation
in the Left Atrial Appendage. This predisposes patients to stroke and other
forms of systemic embolism - Bilateral thrombosis
·
Cardiorenal syndrome 4 in this patient can be
attributed to prior history of heart failure, HTN and age.
·
Abnormal heart rhythms, including atrial
fibrillation or atrial flutter, affect 50 to 60 percent of all patients
over 40 with an ASD.
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
1) Drug name: DOBUTAMINE
MOA: Dobutamine directly
stimulates beta-1 receptors of the heart to increase myocardial contractility
and stroke volume, resulting in increased cardiac output.
Indication: Indicated when
parenteral therapy is necessary for inotropic support in the short-term
treatment of patients with cardiac decompensation due to depressed
contractility resulting either from organic heart disease or from cardiac
surgical procedures.
Efficacy over
dobutamine:
·
P- 673 participants
·
I - dobutamine
·
c - out of 673 participants
random number of patients are given placebo
·
o - dobutamine is not
associated with improved mortality in patients with heart failure, and there is
a suggestion of increased mortality associated with its use
https://go.drugbank.com/drugs/DB00841
https://link.springer.com/article/10.1007/s00134-011-2435-6
2) Drug name: CARVEDILOL
Mechanism of action: Carvedilol inhibits
exercise induce tachycardia through its inhibition of beta adrenoceptors. Carvedilol's action
on alpha-1 adrenergic receptors relaxes smooth muscle in vasculature, leading
to reduced peripheral vascular resistance and an overall reduction in blood
pressure.
Indication: Carvedilol is
indicated to treat mild to severe heart failure, left ventricular
dysfunction after myocardial infarction with
ventricular ejection fraction or hypertension.
Efficacy over
Carvedilol :
·
p : 131
·
i : carvedilol
·
c : out of 131 participants random number of
patients are given placebo
·
o : The beta-blocker carvedilol can be safely
employed in patients with severe heart failure. Improved left ventricular
function
https://go.drugbank.com/drugs/DB01136
https://pubmed.ncbi.nlm.nih.gov/9330125/
3) Drug name: UNFRACTIONED
HEPARIN
MOA: Administered
heparin binds reversibly to ATIII and leads to almost instantaneous
inactivation of factors IIa and Xa The heparin-ATIII complex can also
inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin
is ATIII-dependent. It acts mainly by accelerating the rate of the
neutralization of certain activated coagulation factors by antithrombin, but
other mechanisms may also be involved. The antithrombotic effect of heparin is
well correlated to the inhibition of factor Xa. Heparin is not a thrombolytic
or fibrinolytic. It prevents progression of existing clots by inhibiting
further clotting. The lysis of existing clots relies on endogenous
thrombolytics.
Indication: It is used to
prevent embolisms in patients with atrial fibrillation and as an adjunct
antithrombin therapy in patients with unstable angina and/or non-Q wave
myocardial infarctions
Efficacy over
unfractioned heparin:
·
p : 1473
·
i : unfractioned heparin
·
c : out of 1473 participants random
number of patients are given placebo
·
o : decrase in thromoembolism
https://clinicaltrials.gov/ct2/show/NCT00432796
https://go.drugbank.com/drugs/DB01109
4) Drug name: TAB. DYTOR
MOA: Torasemide is known
to have an effect in the renin-angiotensin-aldosterone system by inhibiting the
downstream cascade after the activation of angiotensin II. This inhibition will
produce a secondary effect marked by the reduction of the expression of
aldosterone synthase, TGF-B1 and thromboxane A2 and a reduction on the
aldosterone receptor binding.
Indication: Torasemide is
indicated for the treatment of edema associated with congestive heart failure,
renal or hepatic diseases.
Efficacy over
dytor:
·
p : 68
·
i : torsemide
·
c : 34
·
o : improvement in peripheral edema
https://pubmed.ncbi.nlm.nih.gov/11862232/
5) Drug name: TAB. TAXIM
MOA: The bactericidal
activity of cefotaxime results from the inhibition of cell wall synthesis via
affinity for penicillin-binding proteins (PBPs). Cefotaxime shows high affinity
for penicillin-binding proteins in the cell wall including PBP Ib and PBP III.
Indication: Used to treat
gonorrhoea, meningitis, and severe infections including infections of the
kidney (pyelonephritis) and urinary system. Also used before an operation to
prevent infection after surgery
Efficacy over Taxim:
·
p : 60
·
i : taxim
·
c : out of 60 participants random number of
patients are given placebo
·
o : the results indicate that cefixime
twice daily is comparable in safety
https://go.drugbank.com/drugs/DB00493
https://pubmed.ncbi.nlm.nih.gov/2663735/
6) Drug name: INJ
THIAMINE
MOA: It is thought that
the mechanism of action of thiamine on endothelial cells is related to a
reduction in intracellular protein glycation by redirecting the glycolytic
flux. Thiamine is mainly the transport form of the vitamin, while the active
forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine
phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP),
also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate
(ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to
their each unique biological functions.
Indication: For the treatment
of thiamine and niacin deficiency states, Korsakov's alcoholic psychosis,
Wernicke-Korsakov syndrome, delirium, and peripheral neuritis.
Efficacy over
thiamine:
·
P : 50
·
I : thiamine
·
C : 25
·
O : Thiamine was not associated to a
significant reduction in vasopressor-free days over 7-days in comparison to
placebo in patients with septic shock
https://go.drugbank.com/drugs/DB00152
https://bmcanesthesiol.biomedcentral.com/articles/10.1186/s12871-020-01195-4
3) What is the
pathogenesis of renal involvement due to heart failure (cardio renal syndrome)?
Which type of cardio renal syndrome is this patient?
Pathogenesis:
The development of CRS mainly focuses on the
inability of the failing heart to generate forward flow, thus resulting in
prerenal hypoperfusion. Inadequate renal afferent flow activates the RAAS, the
sympathetic nervous system, and arginine vasopressin secretion, leading to
fluid retention, increased preload, and worsening pump failure.
The patient is
suffering from Type 4 CRS in which CKD leads to heart failure.
4) What are the
risk factors for atherosclerosis in this patient?
·
Hypertension
·
Bad cholesterol levels
·
Obesity
·
Diabetes
·
Lack of physical activity
·
Age
·
Smoking
5) Why was the
patient asked to get those APTT, INR tests for review?
The patient was
asked to get APTT and INR tests for review as he was prescribed TAB. Acitrom
which is a blood thinner and can cause some common side effects such
as unusual bleeding from the gums, heavy bleeding from cuts or wounds,
unexplained bruising or nosebleeds, heavy periods, abdominal pain, blood
vomiting, bloody or black tarry stools.
Case D:
A 67 year old female patient came to the OPD with C/O shortness of
breath (SOB) since 1/2 hour.
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
12 YEARS AGO
·
Diagnosed with type 2 DM (on medication)
1 YEAR AGO
·
Heartburn like episodes (relieved without any
medication)
7 MONTHS AGO
·
Diagnosed with TB (completed course of medication)
6 MONTHS AGO
·
Diagnosed with HTN (on medication)
NIGHT BEFORE ADMISSION
·
Sweating on exertion
·
Shortness of breath (at rest)
ON THE DAY OF ADMISSION
·
Shortness of breath since 1/2 an hour
ANATOMICAL LOCALISATION
PRIMARY ETIOLOGY:
The increasing
population in older age will lead to greater numbers of them presenting with
acute coronary syndromes (ACS).he elderly are a high risk group with more
significant treatment benefits than younger ACS. Nevertheless, age related
inequalities in ACS care are recognised and persist.
2) What are mechanism of action, indication and efficacy over placebo of
each of the pharmacological and non pharmacological interventions used for this
patient?
1) Drug name: TAB
METFORMIN
MOA: Metformin decreases
blood glucose levels by decreasing hepatic glucose production, decreasing the
intestinal absorption of glucose, and increasing insulin sensitivity by
increasing peripheral glucose uptake and utilization.
Indication: Metformin is
indicated as an adjunct to diet and exercise to increase glycemic control
in adults and pediatric patients 10 years of age and older
diagnosed with type 2 diabetes mellitus.
Efficacy over
Metformin:
·
p : 451
·
i : metformin
·
c : out of 451 participants random number of
patients are given placebo
·
o : Metformin improved glucose variables as
compared with placebo.
https://go.drugbank.com/drugs/DB00331
https://pubmed.ncbi.nlm.nih.gov/9428832/
3) What are the
indications and contraindications for PCI?
Indications of PCI:
·
Acute ST-elevation myocardial
infarction
·
Non–ST-elevation acute coronary
syndrome
· Unstable angina
· Stable angina
· PCI is indicated for
the critical coronary artery stenosis, which does not qualify for CABG
Contraindications of
PCI:
·
High bleeding risk
· Intolerance for oral
antiplatelets long-term
· High-grade chronic
kidney disease
· Critical left main
stenosis with no collateral flow or patent bypass graft
· Chronic total
occlusion of SVG
4) What happens if
a PCI is performed in a patient who does not need it? What are the harms of
overtreatment and why is research on overtesting and overtreatment important to
current healthcare systems?
If PCI is performed
in a patient who doesn't require it then one of the following may occur:
·
Allergic reaction to the dye/contrast
·
Kidney damage from the dye/contrast
·
Injury/tears/ruptures of heart arteries
·
Infection, bleeding or bruising at the catheter
site
·
Blood clots that can lead to stroke or heart attack
·
Retroperitoneal bleeding
Harms of
overtreatment:
·
Psychological stress
·
Financial toxicity
·
Unnecessary care
·
Surgical complications
·
Loss of kidney function
·
Unknown survival benefit
Overtesting, may
cause harm to patients and the healthcare system, including through
misdiagnosis, false positives, false negatives and overdiagnosis. Clinicians
are ultimately responsible for test requests, and are therefore ideally
positioned to prevent overtesting and its unintended consequences.
Case E:
A 60year old Male patient, resident of xxxxxxxx, came to the OPD with
the Chief complaint of chest pain since 3 days and giddiness
and profuse sweating since morning.
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
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
5 DAYS AGO
·
first dose of COVISHEILD vaccine
3 DAYS AGO
·
Mild chest pain in the right side of the
chest - pain was insidious in onset
- gradually progressive
- pain was of dragging
type
- radiating to the back
·
Dizziness was (not increasing or
decreasing with change of position)
·
Profuse sweating
·
Disturbed sleep due to discomfort
ANATOMICAL LOCALISATION
ETIOLOGY OF PATIENTS DISEASE
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
1) Drug name: ASPIRIN
MOA: Blocks prostaglandin
synthesis. It is non-selective for COX-1 and COX-2 enzymes . Inhibition of
COX-1 results in the inhibition of platelet aggregation
Indication: Due to its ability
to inhibit platelet aggregation.
Reducing the risk
of cardiovascular death in suspected cases of myocardial infarction (MI)
Efficacy over
Aspirin:
·
p: 157 248
·
i : aspirin
·
c : out of 157248 participants random number
of patients are given placebo
·
o : Aspirin was associated with a lower
incidence of myocardial infarction. associated with an increased incidence of
major bleeding
https://academic.oup.com/eurheartj/article/40/7/607/5250614
https://go.drugbank.com/drugs/DB00945
2) Drug name: TAB ATROVAS
MOA: Atorvastatin is a
statin medication and a competitive inhibitor of the enzyme HMG-CoA
(3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the
conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol
biosynthesis.
INDICATION : Atorvastatin is
indicated, in combination with dietary modifications, to prevent cardiovascular
events in patients with cardiac risk factors and/or abnormal lipid
profiles. Atorvastatin can be used as a preventive agent for myocardial
infarction, stroke, revascularization, and angina, in patients without coronary
heart disease but with multiple risk factors and in patients with type 2
diabetes without coronary heart disease but multiple risk factors.
Efficacy over
Atrovas:
·
p : 60
·
i: atrovastin
·
c : 42
·
o : Atorvastatin lowered LDL-C, apoB, and
atherogenic lipoprotein subparticles in children with T1D and elevated LDL-C
without worsening insulin resistance. The drug was well tolerated and safe.
Long-term studies would provide better insight on the impact of these
interventions in the development of cardiovascular disease in children with
diabetes.
https://go.drugbank.com/drugs/DB01076
https://pubmed.ncbi.nlm.nih.gov/25418907/
3) Drug name: TAB CLOPIB (active metabolite of
clopidogrel)
MOA: Clopidogrel is
metabolized to its active form by carboxylesterase-1. The active form 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 over Clopib:
·
p : 79,613
·
i : clopidogrel
·
c : out of 79613 subject placebo is
given to random subjects
·
o :clopidogrel was associated with
a highly significant 14% proportional reduction in the risk of cardiovascular
events
https://go.drugbank.com/drugs/DB00758
https://pubmed.ncbi.nlm.nih.gov/19909874/
3) Did the
secondary PTCA do any good to the patient or was it unnecessary?
Percutaneous
transluminal coronary angioplasty is a surgical treatment to reopen a
blocked coronary artery to restore blood flow. It is a type of percutaneous
coronary intervention. When performed on patients with acute myocardial
infarction, it is called primary angioplasty.
After the secondary
PTCA the patient was doing better so it was necessary to do.
Covid-19
CASE-1
Question
1
Interstitial
lung diseases (ILDs) comprise a heterogeneous group of acute and chronic lung
diseases that cause progressive scarring of the lung tissue, compromising
respiratory function and blood oxygenation. The most common form is the
idiopathic pulmonary fibrosis (IPF), which in the vast majority of cases
affects the older population, in a progressive fibrosing manner, resulting in
severe respiratory failure and death within 3–5 years. In patients with
preexisting ILD, COVID-19 infection has led to acute exacerbation of underlying
ILD. The criteria for ILD exacerbation include subacute worsening of dyspnea
and hypoxemia, new pulmonary infiltrates on imaging, and absence of pulmonary
emboli, cardiac failure, and other non-pulmonary causes
Question 2
Steroid therapy
in covid affecting rheumatoid arthritis
There would be
no worsening in RA as we already use corticosteroids in treatment of RA
study provides
all specialists facing the COVID-19 emergency with a very reassuring message
about the possibility of suggesting RMDs patients to continue their current
therapy with ts/bDMARDs without an increased risk and probably with a milder
infection course. Conversely, the use of GC especially a dose > 2.5 mg per
day should be cautiously evaluated during the pandemic.
Steroid therapy
in covid affecting hypothyroidism
Steroids are
used in treatment of hyperthyroidism which can be condition deepening in
hypothyroidism
Question 3
Yes compared to
patients with no autoimmune disorders this patient may have
Question 4
the role of
heparin and low molecular weight (LMW) heparin in this setting has been largely
overlooked. the role of heparan sulfate as a key entry mechanism for
SARS-CoV-2; the efficacy of heparin and LMW heparin in counteracting its entry
into the cell, the recent experimental findings obtained in in vitro studies
using the LMW heparin enoxaparin Inhixa®, the role of heparin and LMW heparin
in modulating the cytokine storm, and the evidence for the use of LMW heparin
in the prevention and treatment of the thromboembolic complications of
COVID-19. The available evidence suggests that LMW heparin appears as a
promising tool in the treatment of COVID-19. Whether its systematic use is
associated with a reduction in complications and ultimately mortality of these
patients is being tested in several studies starting worldwide. the virus
firstly binds to the abundant HS in the extracellular matrix, increasing its
density on the cell surface, and promoting the recognition to its ACE2
receptor. Heparin (100 µg/mL) added 30 min before infection of Vero cells with
SARS-CoV reduced the formation of plaques by 50%.the human coronavirus NL63
similar to SARS-CoV-2 S1 RBD undergoes conformational change upon heparin binding,
and this decreases the adhesion and hence the interaction with the ACE
receptors. Since the interaction with heparan sulfate acts to facilitate ACE
receptors binding by virus, it is also possible to block virus cell entry by
modulating ACE 2 receptors,
CASE-2
Question
1
protein ACE-2
which binds to SARS-Cov-2 and allows the virus to enter human cells is not only
located in the lungs, but also in organs and tissues involved in glucose
metabolism such as the pancreas, the small intestine, the fat tissue, the liver
and the kidney. by entering these tissues, the virus may cause multiple and
complex dysfunctions of glucose metabolism. it is possible that the novel
coronavirus may alter glucose metabolism that could complicate the condition of
preexisting diabetes or lead to new mechanisms of disease.It is said virus infections can also precipitate
type 1 diabetes - a chronic condition in which the pancreas produces little or
no insulin.
Question
2
Yes, In covid
patients with diabetes there is a risk of release of tissue injury-related
enzymes, excessive uncontrolled inflammation responses and hypercoagulable
state associated with dysregulation of glucose metabolism which can lead to
severe pneumonia these patients also show many pathological changes in hrct
scan
Question
3
D dimer -
Pulmonary embolism and deep vein thrombosis were ruled out in patients with
high probability of thrombosis. D-dimer levels significantly increased with
increasing severity of COVID-19 as determined by clinical staging (Kendall’s
tau-b = 0.374, P = 0.000) and chest CT staging role of D dimer is to determine
the severity and reliable prognostic
marker for in-hospital mortality in patients admitted for COVID-19.
It should be
changing management so that anti coagulants or antiplatelet are given to prevent
hemorrhagic/ischemic stroke in the patient
CASE-3
Question
1
Noradrenaline
(norepinephrine) is very effective in raising arterial blood pressure and,
under almost all circumstances, can be titrated to achieve the desired MAP in a
given patient. When given in conscious mammals, renal blood flow is increased
and renal vascular resistance decreased in response to infusion.it increase
organ perfusion and gfr and renal blood flow
in this way it helpful to manage both hypotension and acute kidney
injury at the same time
Question
2
Blood levels of
C-reactive protein (CRP) and lactic dehydrogenase (LDH) at the time of non-ICU
admission for COVID-19 predict likelihood of adverse outcomes, including
development of more serious illness, increased oxygen requirements or ICU
transfer. So finds the first detailed characterization of clinical course among
COVID-19 patients admitted to a non-ICU setting outside a COVID-19 epicenter,
using a remote central monitoring unit (CMU).
“CRP and LDH
blood levels can help stratify risk and prioritize resource allocation for
non-ICU patients with COVID-19”
Question
3
Advantages of
using mechanical ventilation with intubation over other methods include the
humidification of oxygen to prevent dehydration of the airway passages, the
high flow rates can be used to provide carbon dioxide ‘washout’, there is a
reduction in the anatomical dead space and oxygen levels close to 100% can be
delivered.
CASE-4
Question
no 1
ESR –
erythrocyte sedimentation rate
As it is
related to hemoglobin and c reactive protein and c reactive protein increases
in covid infection there was increase in ESR
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