I have been given the following cases to solve in an attmept 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.
This is the link of the questions asked regarding the cases:
https://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.
1) Pulmonology
A) Link to patient details
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html:
1Q) what is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient problem ?
Ans)
Evolution of symptomatology
1st
episode of sob - 20 yr back
2nd
episode of sob - 12 yr back
From
then she has been having yearly episodes for the past 12 yrs
Diagnosed
with diabetes - 8yrs back
Anemia
and took iron injections - 5yr ago
Generalized
weakness - 1 month back
Diagnosed
with hypertension - 20 days back
Pedal
edema - 15 days back
Facial
puffiness- 15 yrs back
Anatomical
location of problem - lungs
Primary
etiology of patient- usage of chulha since 20 yrs might be due to chronic
usage
2Q)
what are the mechanism of action indication and efficacy over placebo of each of
the pharmacological and nonpharmacological interventions used for this
patient?
Ans)
Head end elevation: # MOA;
Improves
oxygenation
Decreases
incidence VAP
Increases
hemodynamic performance
Increases
end expiratory lung volume
Decreases
incidence of aspiration
#Indication:
.head injury
Meningitis
Pneumonia
Oxygen
inhalation to maintain spo2
Bipap
:noninvasive method
MOA:
assist ventilation by delivering positive expiratory and inspiratory
pressure without need for ET incubation
3Q) Cause for current acute exacerbation
Ans) It could be due any infection
4Q) Could the ATT affected her symptoms if so how?
Ans) Yes, ATT affected her symptoms
Isoniazid
and rifampicin -nephrotoxic - raised RFT was seen
2)
Neurology
A) Link to patient details
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
1Q)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans) Evolution of the symptomatology in this patient in terms of an event timeline;
He
had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4
months ago. The most recent time, (4 months ago), he had developed seizures
(most probably GTCS) following cessation of alcohol for 24 hours, which was
associated with restlessness, sweating, and tremors. Following this episode, he
started drinking again.
He
was unable to lift himself off the bed and move around, and had to be assisted.
It was associated with a decrease in food intake since 9 days
He also had short term memory loss since 9 days
The primary etiology of the patient's problem
ALOCHOL
INTAKE
2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans) 1. IVF NS and RL @150ml/hr.
Mechanism of
action;
Sodium
Chloride is source of water and electrolytes. It is capable of inducing
diuresis depending on the clinical condition of the patient. It is a
crystalloid given intravenously in case of shock, dehydration, and diarrhea to
increase the plasma volume.
Indication;
The
following are primary indications for the use of normal saline infusion that
have been approved by the FDA: Extracellular fluid replacement (e.g.,
dehydration, hypovolemia, hemorrhage, sepsis) Treatment of metabolic alkalosis
in the presence of fluid loss. Mild sodium depletion
2. Inj. 1amp
THIAMINE in 100ml NS, TID
Thiamine;
MOA
Mechanism of
Action: Thiamine combines with adenosine triphosphate (ATP) in the liver,
kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate
acts as a coenzyme in carbohydrate metabolism, in transketolation reactions,
and in the utilization of hexose in the hexose-monophosphate shunt.
Indications
and Usage
Thiamine
hydrochloride injection should be used where rapid restoration of thiamine is
necessary, as in Wernicke's encephalopathy, infantile beriberi with acute
collapse, cardiovascular disease due to thiamine deficiency, or neuritis of
pregnancy if vomiting is severe.
3. Inj.
Lorazepam
Mechanism of
action;
Lorazepam
binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated
chloride channel neuron at several sites within the central nervous system
(CNS). It enhances the inhibitory effects of GABA, which increases the
conductance of chloride ions into the cell
Indication;
ATIVAN
Injection is indicated in adult patients for preanesthetic medication,
producing sedation (sleepiness or drowsiness), relief of anxiety, and a
decreased ability to recall events related to the day of surgery.
4. T.
Pregabalin 75mg/PO/ BD
Mechanism of action;
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 in patients 1 month of age and older
5. Inj. HAI
S.C.- premeal
6. GRBS 6th
hourly, premeal: 8am, 2pm, 8pm,2am
7. Lactulose
30ml/PO/BD
Mechanism of action;
Lactulose is
used in preventing and treating clinical portal-systemic encephalopathy. Its
chief mechanism of action is by decreasing the intestinal production and
absorption of ammonia. It has also gained popularity as a potential therapeutic
agent for the management of subacute clinical encephalopathy
INDICATION;
Lactulose is a prescription drug used by mouth or rectally to treat or prevent
complications of liver disease (hepatic encephalopathy). It does not cure the
problem, but may help to improve mental status. Lactulose is a colonic acidifier
that works by decreasing the amount of ammonia in the blood.
8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours
Mechanism of action;
Potassium
ions participate in a number of essential physiological processes, including
the maintenance of intracellular tonicity; the transmission of nerve impulses;
the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of
normal renal function.
INDICATIONS;
Potassium
chloride is used to prevent or to treat low blood levels of potassium
(hypokalemia). Potassium levels can be low as a result of a disease or from
taking certain medicines, or after a prolonged illness with diarrhea or
vomiting.
9. Syp
Potchlor 10ml in one glass water/PO/BD
Mode of
Action ;It helps to maintain potassium balance in the body by restoring normal
potassium levels in patients with a low level of potassium...
3Q)
Why have neurological symptoms appeared this time, that were absent during
withdrawal earlier? What could be a possible cause for this?
Ans) Altered
sensorium due to alcohol withdrawal syndrome, DECREASE LEVEL OF THIAMINE LEADS
TO THE SYMPTOMS
4Q)
What is the reason for giving thiamine in this patient?
Ans)
Thiamine is a key vitamin in the maintenance of membrane integrity and osmotic
gradients across cell membranes and is stored in body tissues predominantly as
thiamine diphosphate (TDP). TDP participates in energy production as an
essential cofactor for several enzymes in the TCA cycle and pentose phosphate
pathways
Thiamine deficiency causes depletion of intracellular TDP, leading to a decreased activity of the TCA cycle and pentose phosphate pathways. Consequently, cellular energy (ATP) depletion and reduction of DNA/RNA and NADPH synthesis ensues, which results in low resistance to oxidative stress. Moreover, there is an accumulation of toxic intermediate metabolic products such as lactate, alanine and glutamate, reduced cellular pH in cells, and disruption of the homeostasis of cellular electrolytes, which results in cytotoxic edema.
B) Link to patient details
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
1Q)
What is the evolution of the symptomatology in this patient in terms of an
event timeline and where is the anatomical localization for the problem and
what is the primary etiology of the patient's problem?
Ans)
The evolution of the symptomatology in this patient in terms of an event
timeline
History
of giddiness
This
was associated with 1 episode of vomiting on the same day.
From
the bed and while walking.
This
was associated with Bilateral Hearing loss, aural fullness and presence of
tinnitus.
He
has associated vomiting- 2-3 episodes per day, non-projectile, non-bilious
containing food particles. Patient has H/o postural instability- he is unable
to walk without presence of supports, swaying is present and he has tendency to
fall while walking
PRIMARY
ETIOLOGY;
Obstruction
of the posterior inferior cerebellar artery (PICA, also the most frequent
location for a cerebellar infarct) leads to a headache and less commonly
vomiting, vertigo, horizontal ipsilateral nystagmus, and truncal ataxia.
Anterior inferior cerebellar artery (AICA) territory infarction more often
leads to dysmetria, Horner's syndrome, unilateral hearing loss and ipsilateral
facial paralysis or anesthesia with contralateral hemi body sensory loss of
pain and temperature. Finally, obstruction of the superior cerebellar artery
(SCA, located most rostral) tends to produce more ataxia, dysarthria, and
nystagmus, with less vertigo, headache, and vomiting. However, presentations
can often be atypical or overlap, in particular for hemorrhagic infarcts.
2Q)
What are mechanism of action, indication and efficacy over placebo of each of
the pharmacological and non-pharmacological interventions used for this patient?
Ans)
Tab Veratin 8 mg PO TID
MECHANISM
OF ACTION;
Betahistine
is one of the few drugs known which is said to improve the microcirculation of
the inner ear. It works as a histamine analogue through 2 modes of action (1)
agonist of H1 receptors and (2) antagonist of H3 receptors. It has a weak
effect on H1 receptors but strong effect on H3 receptors.
INDICATIONS;
Vertin
Tablet is used to prevent and treat a disorder of the inner ear known as
Ménière's disease. The symptoms include dizziness (vertigo), ringing in the
ears (tinnitus), and loss of hearing, probably caused by fluid in the ear.
Inj
Zofer 4 mg IV/TID
Mode
of Action of Zofer
Zofer
Injection works by inhibiting the action of a chemical substance known as
serotonin. Serotonin is responsible for inducing nausea and vomiting.
Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents
vomiting and nausea.
Tab
Ecosprin 75 mg PO/OD
MECHANISM
OF ACTION;
Ecosprin
is an antiplatelet medicine. It works by inhibiting the action of an enzyme,
which makes platelets aggregate together to form a blood clot
INDICATION;
This
tablet is also used to prevent heart attacks, stroke and heart-related chest
pain (angina)
Tab
Atorvastatin 40 mg PO/HS
Mechanism
of Action
Atorvastatin
competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
reductase. By preventing the conversion of HMG-CoA to mevalonate, statin
medications decrease cholesterol production in the liver
INDICATIONS;
Reduce
the risk of non-fatal myocardial infarction.
Reduce
the risk of fatal and non-fatal stroke.
Reduce
the risk for revascularization procedures.
Reduce
the risk of hospitalization for CHF.
Reduce
the risk of angina.
BP
monitoring- 4rth hourly
Tab
Clopidogrel 75 mg PO/OD
MECHANISM
OF ACTION;
The
active metabolite of clopidogrel selectively inhibits the binding of adenosine
diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP-
mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting
platelet aggregation. This action is irreversible.
INDICATIONS;
FDA-approved
indications for clopidogrel include: Use during a percutaneous coronary
intervention (PCI) for acute coronary syndrome (ACS) and stable ischemic heart
disease. Primary prevention of thromboembolism atrial fibrillation
Inj
Thiamine 1 AMP in 100 ml NSPO/BD
Tab
MVT PO/OD
4Q)
Does the patient’s history of alcoholism make him more susceptible to ischemic
or hemorrhagic type of stroke?
Ans) Yes the patient has history of chronic alcoholism and is susceptible to ischemic type of stroke.
C)Link to patient details
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
1Q)
What is the evolution of the symptomatology in this patient in terms of an
event timeline and where is the anatomical localization for the problem and
what is the primary etiology of the patient's problem?
Ans)
Evolution of symptoms: patient was normal 8 months back then developed B/L
pedal edema which gradually progressed.
Aggravated
in sitting and standing position, relived on taking medication
Palpitations:
since 5days, sudden in onset which is more during night Aggravated by lifting
heavy weights, speaking continuously
Dyspnea
during palpitations (NYHA-3) since 5 days
pain:
since 6days, radiating along left upper limb, more during palpitations and
relived on medication.
Chest
pain associated with chest heaviness since 5 days
Etiological
agent:
By
localization, electrolyte imbalance (hypokalemia) causing the her
manifestations like palpitations, chest heaviness, generalized body weakness
Radiating
pain along her left upper limb due to cervical spondylosis
2Q)
What are the reasons for recurrence of hypokalemia in her? Important risk
factors for her hypokalemia?
Ans)
Reason: recurrent hypokalemic periodic paralysis
Current
risk factor: due to use of diuretics
Other
risk factors
A)
Abnormal loses:
Medications-diuretics,
laxatives, enema, corticosteroids
Real
causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis,
hypomagnesaemia
B)
trans cellular shift : alkalosis, thyrotoxicosis, delirium, head injury,
Myocardial, ischemia, recurrent hypokalemic periodic paralysis
C)
Inadequate intake: anorexia, dementia, starvation, total parental nutrition
D)
Psuedohypokalemia: delayed sample analysis, significant leukocytosis
3Q)
What are the changes seen in ECG in case of hypokalemia and associated
symptoms?
Ans)
Changes seen in ECG:
Earliest
change: decreased T-wave amplitude, ST depression, Twave - and inversion or
flat; prolonged PR interval; presence of Uwaves
In
Severe cases: ventricular fibrillation, rarely AV block
Symptoms
of hypokalemia:
Weakness
& fatigue, palpitations, muscle cramps & pain, anxiety, psychosis,
depression, delirium.
D) Link
to patient details
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
Ans) Cells in the brain send electrical signals to one another. The electrical signals pass along your nerves to all parts of the body. A sudden abnormal burst of electrical activity in the brain can lead to the signals to the nerves being disrupted, causing a seizure. This electrical disturbance can happen because of stroke damage in the brain.
A seizure
can affect you in many different ways such as changes to vision, smell and
taste, loss of consciousness and jerking movements.
Seizures after stroke
You’re more
likely to have a seizure if you had a hemorrhagic stroke (bleed on the brain).
Seizures can also be more likely if you had a severe stroke, or a stroke in the
cerebral cortex, the large outer layer of the brain where vital functions like
movement, thinking, vision and emotion take place.
Some people
will have repeated seizures, and be diagnosed with epilepsy. The chances of
this happening may depend on where the stroke happens in the brain and the size
of the stroke.
Pathogenesis
There are
several causes for early onset seizures after ischemic strokes. An increase in
intracellular Ca2+ and Na+ with a resultant lower threshold for depolarization,
glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypo perfusion and hyper perfusion injury
,(particularly after carotid end arterectomy) have all been postulated as
putative neurofunctional etiologies. Seizures after hemorrhagic strokes are
thought to be attributable to irritation caused by products of blood
metabolism. The exact pathophysiology is unclear, but an associated ischemic
area secondary to hemorrhage is thought to play a part. Late onset seizures are
associated with the persistent changes in neuronal excitability and gliotic
scarring is most probably the underlying cause. Hemosiderin deposits are
thought to cause irritability after a hemorrhagic stroke.14 In childhood,
post‐stroke seizures can occur as part of perinatal birth trauma.
Q2) 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?
Ans) Normally the
“consciousness system”—a specialized set of cortical-subcortical
structures—maintains alertness, attention and awareness. Diverse seizure types
including absence, generalized tonic-clonic and complex partial seizures
converge on the same set of anatomical structures through different mechanisms
to disrupt consciousness.
E) Link to patient details
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Q1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Ans) The patient
has minor unattended head injuries in the past 1 yr. According to the CT scan,
the patient has cerebral hemorrhage in the frontal lobe causing probably for
the occurrence of Frontal love ataxia
Q2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?
Ans) The patient
has minor unattended head injuries. During the course of time the minor
hemorrhages if present should have been cured on their own. But the patient is
a chronic alcoholic. This might have hindered the process of healing or might
have stopped the healing rendering it to grow further more into 13 mm sized
hemorrhages occupying Frontal Parietal and Temporal lobes
F) Link to patient details:
Q1) Does the patient’s
history of road traffic accident have any role in his present condition?
Ans) The
closeness of facial bones to the cranium would suggest that there are chances
of cranial injuries. Since the Zygomatic arch and Mandibular process is very
close to the cranium, this might play a role in the patient's present condition
Q)2 What are
warning signs of CVA?
Ans) Weakness or
numbness of the face, arm or leg, usually on one side of the body
Trouble
speaking or understanding
Problems
with vision, such as dimness or loss of vision in one or both eyes
Dizziness or problems with balance or coordination
Problems with movement or walking
Fainting or
seizure
Severe
headaches with no known cause, especially if they happen suddenly
Q3) What is
the drug rationale in CVA?
Ans) Mannitol-
Because of its osmotic effect, mannitol is assumed to decrease cerebral edema.
Mannitol might improve cerebral perfusion by decreasing viscosity, and as a
free-radical scavenger, it might act as a neuroprotection.
Ecospirin
For the
prevention of heart attack, stroke, heart conditions such as stable or unstable
angina (chest pain) due to a blood clot.
Atrovas-Atorva
40 Tablet belongs to a group of medicines called statins. It is used to lower
cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty
substance that builds up in your blood vessels and causes narrowing, which may
lead to a heart attack or stroke.
Rt feed RT
feed is a nursing procedure to provide nutrition to those people who are either
unable to obtain nutrition by mouth or are not in a state to swallow the food
safely.
Q4) Does
alcohol has any role in his attack?
But since
the patient is not a chronic alcoholic and so Alcohol might not have played any
role.
Therefore it
cannot be evaluated without further details
Q5) Does his
lipid profile has any role for his attack??
Ans) The inverse
relationship between serum HDL-C and stroke risk . When taken together it seems
clear that higher baseline levels of serum HDL-C lower the risk of subsequent
ischemic stroke.
Q1) What is myelopathy hand?
Ans) There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
 |
Myelopathy hand sign shown on the right side. There is passive abduction of the fifth finger. This is a sign of pyramidal tract disorder.
Ans) Finger escape
Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".
Q3) What is
Hoffman's sign?
Ans) Hoffman's
sign or reflex is a test used to examine the reflexes of the upper extremities.
This test is a quick, equipment-free way to test for the possible existence of
spinal cord compression from a lesion on the spinal cord or another underlying
nerve condition
Q1) What can
be the cause of her condition ?
Ans)According to MRI cortical vein thrombosis might be the cause of her seizures.
Q2) What are the risk factors for cortical vein thrombosis?
Ans) Infections:
Meningitis,
otitis,mastoiditis
Prothrombotic
states:
Pregnancy,
puerperium,antithrombin deficiency proteinc and protein s deficiency,Hormone
replacement therapy.
Mechanical:
Head
trauma,lumbar puncture
Inflammatory:
SLE,sarcoidosis,Inflammatory
bowel disease.
Malignancy.
Dehydration
Nephrotic
syndrome
Drugs:
Oral
contraceptives,steroids,Inhibitors of angiogenesis
Chemotherapy:Cyclosporine
and l asparginase
Hematological:
Myeloproliferative
Malignancies
Primary and
secondary polycythemia
Intracranial
:
Dural
fistula,
venous
anomalies
Vasculitis:
Behcets
disease wegeners granulomatosis
Q3) There was
seizure free period in between but again sudden episode of GTCS why? Resolved
spontaneously why?
Ans) Seizures are
resolved and seizure free period got achieved after medical intervention but
sudden episode of seizure was may be due to any persistence of excitable foci
by abnormal firing of neurons.
Q4) What drug
was used in suspicion of cortical venous sinus thrombosis?
Ans) Anticoagulants are used for the prevention of harmful blood clots. Clexane ( enoxaparin) low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivates factor xa.
3) Cardiology
A) Link to patient details:
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html
Q1) What is
the difference btw heart failure with preserved ejection fraction and with
reduced ejection fraction?
Ans) The amount of blood pumped out of the heart with each beat is called the ejection fraction (EF). A normal EF is usually around 55 to 70 percent, but it can be lessened in some forms of heart failure.
People with heart failure with reduced ejection fraction (HFrEF) have an EF that is 40 to 50 percent or lower. This is also called systolic heart failure. People with heart failure with preserved ejection fraction (HFpEF) do not have much of a change in their ejection fraction. This is often called diastolic heart failure.
HFrEF were often diagnosed earlier in life and right after a heart attack.
HFpEF were
diagnosed later in life and first experienced symptoms of heart failure between
the ages of 65 and 69. Many of those with HFpEF also shared that they have
other health problems that led to their diagnosis. Many of them also live with
additional health conditions, including acid reflux (GERD), high blood
pressure, kidney disease, and sleep disorders.
HFrEF shared that they feel depressed and/or anxious about their heart failure diagnosis. Risk factors for those in this group include genetics or a family history of heart failure.
HFpEF shared
that they are still able to do the things they enjoyed before their heart
failure diagnosis.risk factors, including:
Sedentary
lifestyle
High blood pressure
Sleep apnea
Other heart
conditions
HFrEF are
more likely to have had surgery, including surgery to implant a pacemaker or
other heart rhythm control device.HFrEF shared that they currently use a
combination therapy to treat their heart failure.
HFpEF have
never had surgery to treat their heart failure or had a device implanted.
HFrEF are
men who live in rural areas.
However,
most respondents with HFpEF are women who live in urban areas.
Q2) Why haven't we done pericardiocenetis in this pateint?
Ans) Pericardiocentesis is done when the pericardial effusion is not resolving on its own . Here the pericardial fluid which has accumulated was resolving on itw own , at the time of admission it was 2.4mm and when discharged it was 1.9 mm . Therefore we did not do pericardiocentesis in this pt.
Q3) What are
the risk factors for development of heart failure in the patient?
Ans) IN THIS PATIENT:
NON
MODIFICABLE:
age
gender
MODIFIABLE:
hypertension
smoking
type 2
diabetes .
kidney
disease.
Q4)What could
be the cause for hypotension in this patient?
Ans) The pt. was anemic with Hb of 8gm/dl . One of the severe complication of anemia is tissue hypoxia which further lead to hypotension.
Ans) obesity
alcohol
diabetes
hypertension
Q2) what is
the reason for anemia in this case?
Ans) 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.
Q3) What is
the reason for blebs and non healing ulcer in the legs of this patient?
Ans) The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type to diabetes mellitus.
Diabetic foot ulcers generally arise as a result of poor circulation in the foot region. While high blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers in many cases.
In cases of poor circulation of blood, the foot ulcers take quite a bit of time to heal as the blood efficiency in the foot region is at a low level. Furthermore, many develop a bit of reduced sensation on the feet as a result of nerve damage or more.
There are many risk factors that may lead to foot ulcers at the end.
Poor quality
or fitting of the footwear.
Unhygienic
appearance of foot.
Improper
care of the nails of the toe.
Heavy intake
of alcohols and tobacco.
Obesity and
Weight-related
Complication
arising from Diabetes like eye problems, kidney problems and more.
Although
aging or old age can also be counted among them.
Q4) What
sequence of stages of diabetes has been noted in this patient?
Ans) alcohol------obesity------impaired glucose
tolerance------diabetes mellitus------microvascular complications like
triopathy and diabetic foot ulcer-------macrovascular complications like
coronary artery disease , coronary vascular disease and peripheral vascular
disease.
Q1) What is
the evolution of the symptomatology in this patient in terms of an event
timeline and where is the anatomical localization for the problem and what is
the primary etiology of the patient's problem?
Ans) the anatomical site is BLOOD VESSELS;
ETIOLOGY: The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans) PHARMACOLOGICAL INTERVENTIONS
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C
mechanism:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.TAB. Digoxin
mechanism:Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart.
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
Q3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans) cardiorenal syndrome type 4 is seen in this patient.
Q4) What are the risk factors for atherosclerosis in this patient?
Ans) effect of hypertention
They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.
Q5) Why was the patient asked to get those APTT, INR tests for review?
Ans) APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule
Q4) 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 overt esting and overtreatment important to current healthcare systems?
Ans) Although PCI is generally a safe procedure, it might cause serious certain complications like :
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye use
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting .
Because of all these complications it is better to avoid PCI in patients who do not require it.
⁃ OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
⁃ Research on overtesting and overtreatment is important as they are more harmful than useful.
Harms to patients
.Performing screening tests in patients with who at low risk for the disease which is being screened.
For example: Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.
.Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations.
.Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant
- OVERDIAGNOSIS.
-Also the adverse effects due to this are more when compared to the benefits.
-Overdiagnosis through overtesting can psychologically harm the patient.
-Hospitalizations[41] for those with chronic conditions who could be treated as outpatients[ can lead to economic burden and a feeling of isolation.
-Harms to health care systems
-The use of expensive technologies and machineries are causing burden on health care systems.
E) Link to patient details:
3 days back
Mild chest pain dragging type and retrosternal pain(radiated)
Anatomical
localisation: Inferior wall of heart
Primary
etiology: Diabetes type 2 (uncontrolled)
High blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels
Q2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
Ans) TAB.
ASPIRIN 325 mg PO/STAT
Mechanism of action: The acetyl group of
acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1
(COX-1) enzyme, leading to irreversible inhibition. This prevents the
production of pain-causing prostaglandins.
TAB ATORVAS
80mg PO/STAT
Mechanism of action: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
TAB CLOPIBB 300mg PO/STAT
Mechanism of action: The active metabolite of clopidogrelselectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
Q3) Did the
secondary PTCA do any good to the patient or was it unnecessary?
Ans) Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty.
Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times
Q1) How did
the patient get relieved from his
shortness of breath after i.v fluids administration by rural medical
practitioner?
Ans) Because of the fluid loss occurred to the patient
there is decreased preload- so, SOB occurred due to decreased CO
IV fluids
administered- there is increased preload- SOB decreased due to better of
cardiac output.
Q2) What is
the rationale of using torsemide in this patient?
Ans) Torsemide used to relieve abdominal distension.
Q3) Was the
rationale for administration of ceftriaxone? Was it prophylactic or for the
treatment of UTI?
Rationale- Used for any bacterial infection.
Q1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans) Evolution of symptomatology
H5 years
back-1st episode of pain abdomen and vomitings
Stopped
taking alcohol for 3 years
1 year back
5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol
again
20 days back
increased consumption of toddy intake
Since 1 week
pain abdomen and vomiting
Since 4 days
fever constipation and burning micturition
Anatomical
localisation: Pancreas and left lung
Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growt factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis
Ans) 1) ING.
MEROPENAM ; TID for 7 days
Meropenem ( broad spectrum Carbepenem ) an antibiotic.
2) ING. METROGYL 500 mg IV TID for 5 days
inj. Metrogyl has METRONIDAZOLE ( Nitroimidazole drug ) an antibiotic
3) ING. AMIKACIN 500 mg IV BD for 5days
It is an Aminoglycoside antibiotic. Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.
4) TPN ( Total Parenteral Nutrition )
* Method of feeding that by passes gastrointestinal tract
* Fluids are given to vein , it provides most of the nutrients body needs.
* TPN has proteins, carbohydrates, fats, vitamins, minerals.
5) IV NS / RL at the rate 12l ml per hour
* Given for fluid replacement ie., treat dehydration
6) ING. OCTREOTIDE 100 mg SC , BD
* It is a Somatostatin long acting analogue.
* It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.
7) ING. PANTOP 40 mg IV , OD
* Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.
8) ING. THIAMINE 100 mg in 100 ml NS IV , TID
* It is B1 supplement.
* It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency
* Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.
9) ING. TRAMADOL in 100 ml NS IV , OD
* It is an opioid analgesic, given to releive pain
Ans) the cause of dyspnea might be PLEURAL EFFUSION
Q2) Name possible reasons why the patient has developed a state of hyperglycemia
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
(i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics
(ii) mitochondrial damage leading to increased release of mAST in serum.
Q4) What is the line of treatment in this patient?
Ans) Plan of action and Treatment:
Investigations:
24 hour urinary protein
Fasting and Post prandial Blood glucose
HbA1c
USG guided pleural tapping
Treatment:
• IVF: 125 mL/hr
• Inj PAN 40mg i.v OD
• Inj ZOFER 4mg i.v sos
• Inj Tramadol 1 amp in 100 mL NS, i.v sos
• Tab Dolo 650mg sos
• GRBS charting 6th hourly
• BP charting 8th hourly
Ans) Differential Diagnosis:
Ruptured Liver Abscess.
Organized collection secondary to Hollow viscous Perforation.
Organized Intraperitoneal Hematoma.
Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
Grade 3 RPD of right Kidney
The most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.
Q2) What was the cause of her death?
Ans) After leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.
Q3) Does her NSAID abuse have something to do with her condition? How?
Ans) NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death
Q2) Reason
for Intermittent Episodes of drowsiness
Ans) Hyponatremia was the cause for his
drowsiness
Q3) why did he
complaint of fleshy mass like passage inurine
Ans) plenty of pus cells in his urine passage appeared as fleshy mass like passage to him
Q4) What are the complications of TURP that he may have had
Ans) Difficulty micturition
Electrolyte imbalances
Infection
Q1) Why is the
child excessively hyperactive without much of social etiquettes ?
Due to the efficacy of medications such as psychostimulants and noradrenergic tricyclics in the treatment of ADHD, neurotransmitters such as dopamine and noradrenaline have been suggested as key players in the pathophysiology of ADHD.
Depressed dopamine activity has been associated with the condition,
Q2) Why doesn't the child have the excessive urge of urination at night time ?
Ans) the child doesn’t have the excessive urge of urination at night time because ADHD is a physcosomatic disorder
Ans) Cough since 2 months on taking food and liquids
difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
laryngeal crepitus- positive
These favour for tracheo esophageal fistula
Q2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.
Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS
1Q) do u
think drinking locally made alcohol
cause liver abscess in this patient due to predisposing factors present in it ?
What could be the cause in this patient?
Ans) yes,
it could be due to intake of contaminated toddy
2Q) what is the etiopathogenesis of liver abscess in a chronic alcoholic patient?(since 30 yrs - 1 bottle/day)
Ans) according to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
3Q) Is liver
abscess is more common in right lobe?
Ans) yes right lobe is involved due to its
more blood supply
4Q) what r
the indications for usg guided
aspiration of liver abscess
Ans) Indications for USG guided aspiration of liver abscess
1. Large abscess more than 6cms
2. Left lobe abscess
3.Caudate
lobe abscess
4. Abscess
which is not responding to drugs
Q1) Cause of
liver abcess in this patient ?
Ans) cause of liver abcess in this patient is ENTAMOEBA HISTOLYTICA
Q2) How do you approach this patient ?
Ans) APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS
Q3) Why do we treat here ; both amoebic and pyogenic liver abcess
Ans) we treat the paient for both amoebic and pyogenic abcess so that we dont rely only on anti-amebic therapy and insure comple treatment of the cause
Q4) Is there a way to confirmthe definitive diagnosis in this patient?
Ans) The confirmatory test for amoebic abcess is
Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).
The diagnosis of amebic liver abscess was based on four or more of the following criteria:
(i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess,
(ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder),
(iii) enlarged and/or tender liver, usually without jaundice,
(iv) raised right dome of the diaphragm on chest radiograph, and
(v) improvement after treatment with antiamebic drugs (e.g., metronidazole).
Q1) 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 aetiology of the patient's problem?
Ans) 3 years ago- diagnosed with hypertension
21 days ago- received vaccination at local PHC which was followed by fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication
18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics)
11 days ago- c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state
4 days ago- a. patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb
b. towards the evening patient periorbital oedema progressed
c. serous discharge from the left eye that was blood tinged
d. was diagnosed with diabetes mellitus
6. patient was referred to a government general hospital
7. patient died 2 days ago
patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was diagnosed with acute oro rhino orbital mucormycosis . rhino cerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes (https://www.cdc.gov/fungal/diseases/mucormycosis/definition. ) the fungus enters the sinuses from the environment and then the brain.
The patient
was also diagnosed with acute infarct in the left frontal and temporal lobe.
Mucormycosis is associated with the occurrence of CVA ( https://journal.chestnet.org/article/S0012-3692(19)33482-8/fulltext#:~:text=There%20are%20few%20incidences%20reported,to%20better%20morbidity%2Fmortality%20outcomes.)
Q2) 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?
The proposed management of the patient was –
1. inj. Liposomal amphotericin B according to creatinine clearance
2. 200mg Iitraconazole was given as it was the only available drug which was
adjusted to his creatinine clearance
3. Deoxycholate was the required drug which was unavailable
https://pubmed.ncbi.nlm.nih.gov/23729001/ this article talks about the efficacy and toxicity of different formulations of amphotericin B
along with the above mentioned treatment for the patient managing others symptoms is also done by-
I. Management of diabetic ketoacidosis –
(a) Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.
(b) Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.
(c) Insulin therapy- Insulin reverses the processes that cause diabetic
ketoacidosis. In addition to fluids and electrolytes, patient will receive
insulin therapy
Q3) What are the postulated reasons for a sudden apparent rise in the
incidence of mucormycosis in India at this point of time?
Ans) Mucormycosis
is may be being triggered by the use of steroids, a life-saving treatment for
severe and critically ill Covid-19 patients. Steroids reduce inflammation in
the lungs for Covid-19 and appear to help stop some of the damage that can
happen when the body's immune system goes into overdrive to fight off
coronavirus. But they also reduce immunity and push up blood sugar levels in
both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing.
10) Medical education
This experience of blogging medicine cases and giving out case opinions and answers to all other patient related questions has been very illuminating and definitely an innovative approach to learning during this pandemic in my opinion. During this period we were given case sheets of the patients to make an attempt and solve them.
I would like to thank Dr. Rakesh Biswas sir and whole medicine department for this wonderful learning opportunity that has been given to us during this ongoing pandemic.
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