CASE-11) Pulmonology
(10 Marks)
A) Link to
patient details:
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.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 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?
4. Could the ATT have
affected her symptoms? If so how?
5.What could be the
causes for her electrolyte imbalance?
1)EVOLUTION
OF EVENTS OF SYMPTOMATOLOGY
1)shortness of breath which is on and off since 20 years.
2)pedal edema since 15 days up to the level of the ankle, pitting
type.
3)facial
puffiness since 15 days
4)drowsiness
since 2 days
5)decreased
urine output since 2 days
Sob
1st
episode of sob 20 years ago (2001) which is sudden in onset and lasted for 1
week. It was relieved on taking medication.
For
next 8 years similar episods of sob for 1 week with no increase in
severity at the same time every year in the month of january-al were
relieved upon medications.
12
years ago another episode of sob,increase in severity that lasted for
20 days d=for which she has been hospitalised and treated
For
the next years-yearly episodes -not mentioned about the severity and duration-?
Latest
episode of sob 30 days ago which was initially grade 2 and then orogressed to
grade 4 which was not relieved on medications and now currently on intermittent
bipap.
Anatomical
localisation of the problem-- in the repiratory system (lungs) and
cariovascular system(heart)
PRIMARY
ETIOLOGY OF THE PATIENT PROBLEM -
Acute exacerbation of COPD associated with right heart failure
and bronchiectasis.
2)MECHANISM
OF ACTION, INDICATION AND EFFICACY OF THE INTERVENTIONS
- HEAD END
ELEVATION 30/45DEGREES - USED IN MECHANICALLY VENTILATED PEOPLE FOR
DECREASING INCIDENCE OF ASPIRATION AND VENTILATOR ASSOCIATED PNEUMONIA.
IT ALSO SHOWN TO IMPROVE OXYGENATION AND HEMODYNAMIC PERFORMANCE.
- O2 inhalation to
maintain SPO2 above 92%
- Intermittent
BiPAP for 2hrs TO SUPPORT VENTILATION
- Inj. AUGUMENTIN
1.2gm IV BO
- TAB.
AZITHROMYCIN 500mg OD
- INJ. LASIX IV BO
if SBP greater than 110 mmHg
- TAB PANTOP 40mg
PO OD
- INJ.
HYDROCORTISONE 100 mg IV
- NEB. with
IPRAVENT, BUDECORT 6 hrly
- TAB PULMOCLEAR
100 mg PO OD
- chest
physiotherapy
- GRBS 6 hrly
- INJ. HAI SC ( 8
am- 2pm- 8pm)
- Temp, BP, PR,
SPO2 monitoring
- I/O charting
- INJ. THIAMINE 1
amp in 100 ml of NS.
2)
Neurology (10 Marks)
A) Link
to patient details:
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
(1) What
is the evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
Ans) Type 2 DM - since 2 YRS
Seizures (2-3 eps) - 1month ago
Seizures -4months ago
Short term memory loss -9 days ago
Started talking - 9days ago
Started laughing -9 days ago
He was unable to lift himself off bed - since
9 days
Decreased food intake - since 9days
General body pains -1 day ago
Anatomical
localisation :- brain (prefrontal cortex,hypothalamus & limbic system)
Primary etiology :-
alcohol
(2) What are mechanism of
action, indication and efficacy over placebo of each of the
pharmacological and non
pharmacological interventions used for this patient?
Ans) RL & NS :-
Electrolyte replenishment
Thiamine :-
moa:- combines with ATP in liver , kidney & leucocytes produces thiamine
diphosphate which axts as a coenzyme incarbohydrate metabolism in
transketolation
Indication :- for
low levels of thiamine. For digestive problems (alcoholics have thiamine deficiency)
Lorazepam:- moa
:- lorazepam binds to benzodiazepine receptors on postsynaptic GABA-A
ligand gated clorine channel neuron at several sites within the CNS. It
Inhibits the effects of GABA which increases the conductance of chlorine
ions into the cell
Indication :-
anxiety disorfers with/ without depression symptoms
Pregabakin :-
moa :- it may reduce excitatory neurotransmitter release by binding to the
α2-δ protein subunit of voltage-gated calcium channels
(3) Why have neurological
symptoms appeared this time, that were absent during withdrawal earlier?
What could be a possible
cause for this?
Ans) Excessive drinking excites and irritates
N.S
Body will be dependent on daily basis for
alcohol
CNS cannot adapt without alcohol
Cessation of alcohol leads to alcohol
withdrawal symptoms.
(4) What is the reason
for giving thiamine in this patient?
Ans)Alcoholics have thiamine deficiency. As
the patient decreased his food intake since 9days ge has been diagnosed as
thiamine deficiency as thiamine is not produced in our body.
Thiamine is administered to the patient in
order to keep the nervous system healthy
(5) What is the probable reason for kidney
injury in this patient?
Ans) DEHYDRATION
(6). What is the probable
cause for the normocytic anemia?
Ans) kidney failure - as erythropoeitin is
produced in kidney which plays a key role in the production of RBCs
(7) Could chronic alcoholism have
aggravated the foot ulcer formation? If yes, how and why
Ans) yes, it has aggrevated the foot ulcer
formation due to anaemia caused by alcoholism
B) Link
to patient details:
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?
|
· 1) history of giddiness 7 days back.
It started at around 7 am when the patient was doing his usual morning
routine. He suddenly felt giddy and took rest, after which it subsided
briefly. · This was associated with 1 episode of
vomiting on the same day. - He then developed giddiness, that was
sudden in onset, continuous and gradually progressive. It increased in
severity upon getting up from the bed and while walking. - 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 |
- then pt developed slurring of speech and deviation of mouth 2
days back.
ANTOMICAL
LOCALIZATION OF THE PROBLEM;
It
is localised to the cerebellum.
Primary
etiology of the pts problem;
Infarction
in the right inferior cerebellar hemisphere.
2)PHARMACOLOGICAL
INTERVENTION;
-Tab
Veratin 8 mg PO TID-As pt has history of vomitings-it s indicated.
VERTIN
8MG TABLET comes under the category of medications called 'antihistamine
anti-vertigo medication', primarily indicated in the treatment of Meniere’s
disease and its symptoms including dizziness (vertigo), ringing in the ears
(tinnitus), feeling sick (nausea), and difficulty in hearing. Meniere’s disease
is a medical condition that affects the inner ear caused by the building up of
extra fluid inside the ear. In vertigo, a person feels that they are moving or
spinning, but they are not moving. In tinnitus, a person feels a noise or
ringing in their ears.
VERTIN 8MG TABLET compromises of Betahistine
that works by enhancing the blood flow to the affected part of the ear and also
by reducing the amount of fluid in the inner ear. This drug also reduces the
number of attacks a person can have.
VERTIN
8MG TABLET may cause some of the unpleasant effects that include feeling sick
(nausea), indigestion (acid reflux), bloating or mild stomach ache, headache.
Most of the unpleasant effects caused by this medicine do not require
medical attention and will go in a couple of days. However, if the side effects
get worsen with time or do not pass in a couple of days, then one should seek
medical help.
-Inj
Zofer 4 mg IV/TID- it contains ondensetron, an anti emetic drug.
Tab
Ecosprin 75 mg PO/OD
.Initial manifestations of acute cerebral ischemia, such as
ischemic stroke and transient ischemic attack (TIA), are often followed by
recurrent vascular events, including recurrent stroke.2 To
reduce this burden, antiplatelet therapy is a key component of the management
of noncardioembolic ischem
Tab
Atorvostatin 40 mg PO/HS- to improve lipid profile
BP
monitoring- 4rth hourly as he was diagnosed with denovo hpertension
Tab
Clopidogrel 75 mg PO/OD
Clopidogrel
reduces the stickiness of platelets, and this helps prevent the platelets from
sticking to the inside of an artery and forming a thrombus. This reduces the
risk of you having a heart attack or stroke.
Inj
Thiamine 1 AMP in 100 ml NSPO/BD
Tab MVT
PO/OD-
Thiamine
plays an important role in helping the body convert carbohydrates and fat into
energy. It is essential for normal growth and development and helps to maintain
proper functioning of the heart and the nervous and digestive systems.
For the
treatment of thiamine and niacin deficiency states, Korsakov's alcoholic
psychosis, Wernicke-Korsakov syndrome, delirium, and peripheral neuritis.
ADVICE
ON DISCHARGE-
Tab
Vertin 8 mg PO TID - 1 week
Tab
Zofer 4 mg IV/TID - 1 week
Tab
Ecosporin 75 mg PO/OD - 1 week
Tab
Atorvostatin 40 mg PO/HS - 1 week
Tab
Clopidogrel 75 mg PO/OD - 1 week
Tab MVT
PO/OD - 1 week
- 3)HSTORY
OF DENOVO HYPERTENSION;
- history
of deovo hypertension has a huge role to play . As hypertension has a huge
role in the pathogenesis of cerebrovascular accident.
Acute
ischaemic strokes occur due to an occlusion of an intracranial or cervical
artery with consequent deprivation of blood and oxygen to a brain territory. A
few minutes after an arterial occlusion in the brain, a core ischaemic lesion
is established, however a larger area at risk of hypoperfusion can be
salvageable if recanalisation therapies are administered. The salvageable area or
ischaemic penumbra is largely dependent on collateral blood flow and acute
reductions of BP can threaten perfusion in critical areas.[25]
In the
acute phase of ischaemic stroke, early initiation or resumption of
antihypertensive treatment is indicated only in patients treated with
recombinant tissue-type plasminogen activator or if hypertension is
extreme.
C) Link to patient details:
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?
1)EVOLUTION
OF SYMPTOMATOLOGY;
10 yrs back had the
episode of paralysis of both upper and lowerlimbs(rt and left)
(right and left)paresis
due to hypokalemia 1year back
:
*Swelling over the legs(bilateral)-8
months-gradually progressing and it is present both in sitting and standing
position and relieved on taking medication.
blood
infection -7 months back
Neck
pain -since 2 months.
Pain along her left upper limb associated with
tingling and numbness-6 days
Chestpain -since5 days
*Difficulty in breathing-5 days
Palpitations: since
5days-which are sudden in onset,more during night time and aggregated by
lifting weights, speaking continuously and it is relieved by drinking more water,
medication
*dyspnoea during palpitations
(NYHA-CLASS-3)-since5 days.
ANATOMICAL LOCALIZATION
OF THE PROBLEM;
CERVICAL VERTEBRAE AND ELECTROLYTE IMBALANCE
PRIMARY ETIOLOGY OF THE
PATIENT;
CERVICAL SPONDYLOSIS AND RECURRENT HYPOKALEMIC
PERALYSIS.
2)causes for recurrent hypokalemia in
this patient may be due to inadequate intake of potassium or due to excess loss
of potassium in the urine.
Other causes of hypokalemia;
Causes
of hypokalemia.
|
Gastrointestinal
tract losses |
•
Chronic diarrhea, including chronic laxative abuse and bowel diversion |
|
Intracellular
shift |
•
Glycogenesis during total parenteral nutrition or enteral hyperalimentation
(stimulating insulin release) |
|
Renal
potassium losses |
•
Adrenal steroid excess (Cushing’s syndrome) |
|
Drugs |
•
Thiazides |
IMPORTANT RISKFACTORS FOR HYPOKALEMIA;
The riskfactors in her are;
female gender,
poor potassium diet.
other riskfactors include;
·
Medications like diuretics
·
Low BMI
·
Diarrhea, cushing syndrome,
and any condition that cause increase potassium loss
3) ECG
CHANGES IN HYPOKALEMIA AND ASSOCIATED SYMPTOMS;
The ECG
in hypokalemia may appear normal or may have only subtle findings immediately
before clinically significant dysrhythmias. ECG findings may include the
following:
·
Ventricular dysrhythmia
·
Prolongation of QT interval [53]
·
ST-segment depression
·
T-wave flattening
·
Appearance of U waves
·
Ventricular arrhythmias (eg, premature ventricular contractions
[PVCs], torsade de pointes, ventricular fibrillation) [54]
·
Atrial arrhythmias (eg, premature atrial contractions [PACs],
atrial fibrillation)
SYMPTOMS;
The
symptoms of hypokalemia are nonspecific and predominantly are related to
muscular or cardiac function.
Weakness
and fatigue are the most common complaints.
The muscular
weakness that occurs with hypokalemia can manifest in protean ways (eg,
dyspnea, constipation or abdominal distention, exercise intolerance).
Rarely,
muscle weakness progresses to frank paralysis. With severe hypokalemia or total
body potassium deficits, muscle cramps and pain can occur with rhabdomyolysis.
Occasionally,
a patient may complain of worsening diabetes control or polyuria due to a
recent onset of hyperglycemia or nephrogenic diabetes insipidus.
Patients
also may complain of palpitations.
Psychological
symptoms may include psychosis, delirium, hallucinations, and depression.
D) Link
to patient details:
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?
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?
)Seizures
are changes in the brain’s electrical activity. These changes can cause
dramatic, noticeable symptoms, or in other cases no symptoms at all.
The brain
consists of nerve cells that communicate with each other through electrical
activity. A seizure occurs when one or more parts of the brain has a burst of
abnormal electrical signals that interrupt normal brain signals. Anything that
interrupts the normal connections between nerve cells in the brain can cause a
seizure. This includes a high fever, high or low blood sugar, alcohol or drug
withdrawal, or a brain concussion. But when a person has 2 or more seizures
with no known cause, this is diagnosed as epilepsy.
There are
different types of seizures. The type of seizure depends on which part and how
much of the brain is affected and what happens during the seizure. The 2 main
categories of epileptic seizures are focal (partial) seizure and generalized
seizure.
Focal
(partial) seizures
Focal
seizures take place when abnormal electrical brain function occurs in one or
more areas of one side of the brain. Before a focal seizure, you may have an aura,
or signs that a seizure is about to occur. This is more common with a complex
focal seizure. The most common aura involves feelings, such as deja vu,
impending doom, fear, or euphoria. Or you may have visual changes, hearing
abnormalities, or changes in your sense of smell. The 2 types of focal seizures
include:
Simple
focal seizure
The
symptoms depend on which area of the brain is affected. If the abnormal
electrical brain function is in the part of the brain involved with vision
(occipital lobe), your sight may be altered. More often, muscles are affected.
The seizure activity is limited to an isolated muscle group. For example, it
may only include the fingers, or larger muscles in the arms and legs. You may
also have sweating, nausea, or become pale. You don’t lose consciousness in
this type of seizure.
Complex
focal seizure
This type
of seizure often occurs in the area of the brain that controls emotion and
memory function (temporal lobe). You will likely lose consciousness. This may
not mean you pass out. You may just stop being aware of what's going on around
you. You may look awake, but have a variety of unusual behaviors. These may
range from gagging, lip smacking, running, screaming, crying, or laughing. You
may be tired or sleepy after the seizure. This is called the postictal period.
Generalized
seizure
A
generalized seizure occurs in both sides of the brain. You will lose
consciousness and be tired after the seizure (postictal state). Types of
generalized seizures include:
Absence
seizure
This is
also called petit mal seizure. This seizure causes a brief changed state of
consciousness and staring. You will likely maintain your posture. Your mouth or
face may twitch or your eyes may blink rapidly. The seizure usually lasts no longer
than 30 seconds. When the seizure is over, you may not recall what just
occurred. You may go on with your activities as though nothing happened. These
seizures may occur several times a day.
Atonic
seizure
This is
also called a drop attack. With an atonic seizure, you have a sudden loss of
muscle tone and may fall from a standing position or suddenly drop your head.
During the seizure, you will be limp and unresponsive.
Generalized
tonic-clonic seizure (GTC)
This is
also called grand mal seizure. The classic form of this kind of seizure has 5
distinct phases. Your body, arms, and legs will flex (contract), extend
(straighten out), and tremor (shake). This is followed by contraction and
relaxation of the muscles (clonic period) and the postictal period. During the
postictal period, you may be sleepy. You may have problems with vision or
speech, and may have a bad headache, fatigue, or body aches. Not all of these
phases occur in everyone with this type of seizure.
Myoclonic
seizure
This type
of seizure causes quick movements or sudden jerking of a group of muscles.
These seizures tend to occur in clusters. This means that they may occur
several times a day, or for several days in a row.
-YES,there
is relation between the occurance of seizures and brain stroke.
RELATION
BETWEEN BRAINSTROKE AND SEIZURE;
2).
During previous episodes propagation of seizure activity may be confined to the
sensorimotor areas bilaterally while sparing the neural structures involved in
maintaining consciousness and in processing language and memory.
But in
the last episode, it might involve the neurosensory areas that involve
consciousness as CT report has shown that there is old infarct with gliosis in
the temporal and occipital lobes.
E) Link
to patient details:
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?
2) What
was the reason for his IC bleed? Does Alcoholism contribute to bleeding
diatheses ?
1) REASON FOR THIS PATIENT TO DEVELO[P ATAXIA
;
Ataxia
describes a lack of muscle control or coordination of voluntary movements, such
as walking or picking up objects. A sign of an underlying condition, ataxia can
affect various movements and create difficulties with speech, eye movement and
swallowing.
This
patient developed persistent ataxia during past one year due to stroke in
frontal, parietal and temporal lobes which are resulted due to head trauma that
were left untreated.
other
causes of ataxia;
Damage,
degeneration or loss of nerve cells in the part of your brain that controls
muscle coordination (cerebellum), results in ataxia. Your cerebellum comprises
two portions of folded tissue situated at the base of your brain near your
brainstem. This area of the brain helps with balance as well as eye
movements, swallowing and speech.
Diseases
that damage the spinal cord and peripheral nerves that connect your cerebellum
to your muscles also can cause ataxia. Ataxia causes include:
·
Head trauma. Damage to your brain
or spinal cord from a blow to your head, such as might occur in a car accident,
can cause acute cerebellar ataxia, which comes on suddenly.
·
Stroke. Either a blockage or
bleeding in the brain can cause ataxia. When the blood supply to a part of your
brain is interrupted or severely reduced, depriving brain tissue of oxygen and
nutrients, brain cells die.
·
Cerebral palsy. This
is a general term for a group of disorders caused by damage to a child's brain
during early development — before, during or shortly after birth — that affects
the child's ability to coordinate body movements.
·
Autoimmune diseases. Multiple
sclerosis, sarcoidosis, celiac disease and other autoimmune conditions can
cause ataxia.
·
Infections. Ataxia can be an
uncommon complication of chickenpox and other viral infections such
as HIV and Lyme disease. It might appear in the healing stages of the
infection and last for days or weeks. Normally, the ataxia resolves over time.
·
Paraneoplastic syndromes. These
are rare, degenerative disorders triggered by your immune system's response to
a cancerous tumor (neoplasm), most commonly from lung, ovarian, breast or
lymphatic cancer. Ataxia can appear months or years before the cancer is
diagnosed.
·
Abnormalities in the brain. An
infected area (abscess) in the brain may cause ataxia. A growth on the brain,
cancerous (malignant) or noncancerous (benign), can damage the cerebellum.
·
Toxic reaction. Ataxia
is a potential side effect of certain medications, especially barbiturates,
such as phenobarbital; sedatives, such as benzodiazepines; antiepileptic drugs,
such as phenytoin; and some types of chemotherapy. Vitamin B-6 toxicity also
may cause ataxia. These causes are important to identify because the effects
are often reversible.
Also, some medications you
take can cause problems as you age, so you might need to reduce your dose or
discontinue the medication.
Alcohol and drug
intoxication; heavy metal poisoning, such as from lead or mercury; and solvent
poisoning, such as from paint thinner, also can cause ataxia.
·
Vitamin E, vitamin B-12 or thiamine deficiency. Not
getting enough of these nutrients, because of the inability to absorb enough,
alcohol misuse or other reasons, can lead to ataxia.
·
Thyroid problems. Hypothyroidism
and hypoparathyroidism can cause ataxia.
·
COVID-19 infection. This
infection may cause ataxia, most commonly in very severe cases.
For some
adults who develop sporadic ataxia, no specific cause can be found. Sporadic
ataxia can take a number of forms, including multiple system atrophy, a
progressive, degenerative disorder.
Hereditary ataxias
Some
types of ataxia and some conditions that cause ataxia are hereditary. If you
have one of these conditions, you were born with a defect in a certain gene
that makes abnormal proteins.
The
abnormal proteins hamper the function of nerve cells, primarily in your
cerebellum and spinal cord, and cause them to degenerate. As the disease
progresses, coordination problems worsen.
You can
inherit a genetic ataxia from either a dominant gene from one parent (autosomal
dominant disorder) or a recessive gene from each parent (autosomal recessive
disorder). In the latter case, it's possible neither parent has the disorder
(silent mutation), so there might be no obvious family history.
Different
gene defects cause different types of ataxia, most of which are progressive.
Each type causes poor coordination, but each has specific signs and symptoms.
Autosomal dominant ataxias
Autosomal dominant
inheritance pattern
Open
pop-up dialog box
These
include:
·
Spinocerebellar ataxias. Researchers
have identified more than 40 autosomal dominant ataxia genes, and the number
continues to grow. Cerebellar ataxia and cerebellar degeneration are common to
all types, but other signs and symptoms, as well as age of onset, differ
depending on the specific gene mutation.
·
Episodic ataxia (EA). There
are eight recognized types of ataxia that are episodic rather than progressive
— EA1 through EA7, plus late-onset episodic ataxia. EA1
and EA2 are the most common. EA1 involves brief ataxic episodes that
may last seconds or minutes. The episodes are triggered by stress, being startled
or sudden movement, and often are associated with muscle twitching.
EA2 involves longer
episodes, usually lasting from 30 minutes to six hours, which also are
triggered by stress. You might have dizziness (vertigo), fatigue and muscle weakness
during your episodes. In some cases, symptoms resolve in later life.
Episodic ataxia doesn't
shorten life span, and symptoms might respond to medication.
Autosomal recessive ataxias
Autosomal recessive
inheritance pattern
Open
pop-up dialog box
These
include:
·
Friedreich's ataxia. This
common hereditary ataxia involves damage to your cerebellum, spinal cord and
peripheral nerves. Peripheral nerves carry signals from your brain and spinal
cord to your muscles. In most cases, signs and symptoms appear well before age
25.
The rate of disease
progression varies. The first indication generally is difficulty walking (gait
ataxia). The condition typically progresses to the arms and trunk. Muscles
weaken and waste away over time, causing deformities, particularly in your
feet, lower legs and hands.
Other signs and symptoms
that might develop as the disease progresses include slow, slurred speech
(dysarthria); fatigue; rapid, involuntary eye movements (nystagmus); spinal
curvature (scoliosis); hearing loss; and heart disease, including heart
enlargement (cardiomyopathy) and heart failure. Early treatment of heart
problems can improve quality of life and survival.
·
Ataxia-telangiectasia. This
rare, progressive childhood disease causes degeneration in the brain and other
body systems. The disease also causes immune system breakdown (immunodeficiency
disease), which increases susceptibility to other diseases, including
infections and tumors. It affects various organs.
Telangiectasia is the
formation of tiny red "spider" veins that might appear in the corners
of your child's eyes or on the ears and cheeks. Delayed motor skill
development, poor balance and slurred speech are typically the first
indications of the disease. Recurrent sinus and respiratory infections are
common.
Children with
ataxia-telangiectasia are at high risk of developing cancer, particularly
leukemia or lymphoma. Most people with the disease need a wheelchair by their
teens and die before age 30, usually of cancer or lung (pulmonary) disease.
·
Congenital cerebellar ataxia. This
type of ataxia results from damage to the cerebellum that's present at birth.
·
Wilson's disease. People
with this condition accumulate copper in their brains, livers and other organs,
which can cause neurological problems, including ataxia. Early identification
of this disorder can lead to treatment that will slow progression.
2) REASON
FOR IC BLEEDING AND ALCOHOL CONTRIBUTION;
IC
BLEEDING might be due to the 1) HEAD TRAUMA as he has history of falls
when inebriated.
2)RUPTURE
OF ANEURYSM OR
3)
OVERINTAKE OF ALCOHOL DURING THE PAST 3 YEARS.
4)Buildup
of fatty deposits in the arteries (atherosclerosis).
5)Blood
clot that formed in the brain or traveled to the brain from another part of the
body, which damaged the artery and caused it to leak.
6)Buildup
of amyloid protein within the artery walls of the brain (cerebral amyloid
angiopathy).
7)A
leak from abnormally formed connections between arteries and veins (arteriovenous
malformation).
8)Bleeding
disorders- PT AND APTT RESULTS-?
9)Conditions
related to abnormal collagen formation in the blood vessel walls that can cause
to walls to be weak, resulting in a rupture of the vessel wall.
ALCOHOL
CONTRIBUTION IN BLEEDING DIATHESIS;
Blood
clotting, or coagulation, an important physiological process that ensures the
integrity of the vascular system, involves the platelets, or thrombocytes,4 as
well as several proteins dissolved in the plasma. When a blood vessel is
injured, platelets are attracted to the site of the injury, where they
aggregate to form a temporary plug. The platelets secrete several proteins
(i.e., clotting factors) that—together with other proteins either secreted by
surrounding tissue cells or present in the blood—initiate a chain of events
that results in the formation of fibrin. Fibrin is a stringy protein that forms
a tight mesh in the injured vessel; blood cells become trapped in this mesh,
thereby plugging the wound. Fibrin clots, in turn, can be dissolved by a
process that helps prevent the development of thrombosis (i.e., fibrinolysis).
Alcohol can interfere with these processes at several levels, causing, for
example, abnormally low platelet numbers in the blood (i.e., thrombocytopenia),
impaired platelet function (i.e., thrombocytopathy), and diminished
fibrinolysis. These effects can have serious medical consequences, such as an
increased risk for strokes.
Thrombocytopenia
is a frequent complication of alcoholism, affecting 3 to 43 percent of
nonacutely ill, wellnourished alcoholics and 14 to 81 percent of acutely ill,
hospitalized alcoholics.
The exact
mechanisms underlying alcohol-related thrombocytopenia remain unknown. Some
researchers have suggested that alcohol intoxication itself, rather than
alcohol-related nutritional deficiencies, causes the decrease in platelet
numbers. This view is supported by findings that thrombocytopenia developed in
healthy subjects who received a diet containing adequate protein and vitamin
levels (including large doses of folic acid) and consumed the equivalent of 1.5
pints (i.e., 745 milliliters) of 86-proof whiskey for at least 10 days
(Lindenbaum 1987). The subjects’ platelet levels returned to normal when alcohol
consumption was discontinued. Similarly, platelet counts can be reduced in
well-nourished alcoholics who do not suffer from folic acid deficiency. The
available data also suggest that alcohol can interfere with a late stage of
platelet production as well as shorten the life span of existing platelets.
Individual drinkers appear to differ in their susceptibility to alcohol-induced
thrombocytopenia. Thus, clinicians have noted that some people who consume
alcohol in excess repeatedly develop thrombocytopenia (often severely), whereas
other drinkers maintain normal platelet levels. In addition to differences in
the quantity of alcohol consumed, inherited or acquired variations in an
individual drinker’s biochemistry may account for these differences in susceptibility.
Thrombocytopathy Alcohol affects not only platelet production but also platelet
function. Thus, patients who consume excessive amounts of alcohol can exhibit a
wide spectrum of platelet abnormalities when admitted to a hospital. These
abnormalities include impaired platelet aggregation, decreased secretion or
activity of platelet-derived proteins involved in blood clotting, and
prolongation of bleeding in the absence of thrombocytopenia. Because alcohol
impairs the function of the normal blood-clotting system, it also can adversely
interact with over-the-counter and prescription medications that prolong
bleeding or prevent coagulation. For example, alcohol can potentiate the
prolongation of bleeding time caused by aspirin and other nonsteroidal anti-inflammatory
drugs (NSAID’s) (e.g., ibuprofen or indomethacin), particularly when alcohol
ingestion equivalent to about four drinks occurs simultaneously with or
following ingestion of normal doses of these medications. As a result, the
concomitant use of alcohol and aspirin or NSAID’s greatly increases the
patient’s risk for gastrointestinal bleeding. Similarly, alcohol can enhance
aspirin-induced fecal blood loss.
Fibrinolysis
The body’s ability to prevent excessive bleeding using the coagulation system
is balanced by the fibrinolytic system, which helps ensure blood flow in
peripheral organs and tissues by dissolving inappropriate fibrin clots.
Alcohol’s effect on fibrinolysis is controversial. Whereas some older studies
reported an increase in fibrinolytic activity after alcohol consumption, more
recent, better controlled studies have demonstrated that alcohol diminishes
fibrinolysis the day after alcohol ingestion or during prolonged alcohol
consumption. These observations suggest that alcoholics may be at increased
risk for thrombosis.
Alcohol-induced
impairment of the blood-clotting and/or fibrinolytic systems can have serious
medical consequences. Most significantly, clinical epidemiological data suggest
that a recent bout of heavy drinking increases the drinker’s risk of suffering
a hemorrhagic or ischemic stroke. During a hemorrhagic stroke, the blood flow
to a brain area is impaired due to a ruptured blood vessel that results in
bleeding in the brain. If the blood flow is interrupted because a blood vessel
is blocked by a blood clot, the condition is called an ischemic stroke. Alcohol
conceivably can contribute to both conditions by interfering with the normal
coagulation system and by reducing fibrinolysis, respectively.6 For example,
researchers have suggested that acetaldehyde interacts with some proteins of
the blood-clotting system and thus induces abnormal coagulation. In addition to
these direct effects on the blood components, alcohol may increase the risk of
a stroke indirectly by altering the drinker’s blood pressure; heart rate; tone
of the heart muscles; and “thickness,” or viscosity, of the blood .
F) Link
to patient details:
Questions
1.Does
the patient's history of road traffic accident have any role in his
present condition?
2.What
are warning signs of CVA?
3.What
is the drug rationale in CVA?
4. Does
alcohol has any role in his attack?
5.Does
his lipid profile has any role for his attack??
shivani reddy case
1)yes, the pt history of cva has major
role in the development of the disease. there is dislocation of the shoulder,
mandible and zygomatic in that accident. there might be damage to the middle
cerebral artery that may went unnoticed initially.
Areas supplied by
the middle cerebral artery include: The bulk of the lateral
surface of the hemisphere; except for the superior inch of the frontal and parietal
lobe (anterior cerebral artery), and the inferior part of the
temporal lobe.
and now in the ct we can see the altered
signal intensity in the areas involving the left caudate nucleus,lentiform
nucleus,left frontal and left temporal areas.
2) signs of cva in this pt are;
1. WEAKNESS OF RIGHT
UPPERLIMB AND LOWER LIMB SINCE ONE DAY.
2.DEVIATION OF MOUTH
TOWARDS LEFT SINCE ONE DAY.
the other signs of cva could be ;
. Since the body is affected on the
opposite side of where the stroke occurs in the brain, having one-sided
facial drooping or weakness on one side of the body is common. The most
frequently observed indicators in an emergency setting are the following:
- Facial drooping, typically on
one side of the face
- Vision loss in
one eye, or blurred or double vision
- Weakness or
numbness on one side of the body
- Lack of movement or
sensation on one side of the body
- Loss of balance
- Slurred speech or
absence of speech
- Altered level of consciousness
- 3) drug rationale in cva;
- 1.Injection Mannitol
100ml/IV/TD -it is an osmotic diuretic. it is used to decrease the
cerebral edema. MOA--
- 2.TAB Ecospirin 75 mg po/OD aspirin,
irreversibly inactivates platelet cyclooxygenase, which is responsible for
prostaglandin and thromboxane synthesis.5 In
particular, aspirin irreversibly blocks production of thromboxane A2.6 Thromboxane
A2 is a potent platelet activator and proaggregant; hence by blocking
thromboxane A2 synthesis, ASA is able to achieve an antiplatelet effectic
stroke and TIA.3
.Initial
manifestations of acute cerebral ischemia, such as ischemic stroke and
transient ischemic attack (TIA), are often followed by recurrent vascular
events, including recurrent stroke.2 To
reduce this burden, antiplatelet therapy is a key component of the management
of noncardioembolic ischem
3.TAB
ATORVAS 40mg po/HS
4.BP/PR/TEMP/SP02
MONITORING (4th hourly)- vitals should monitored regularly
5.RT FEEDS-100ml milk with protein powder(2nd hourly)Ryle'sTube
feeding is given to the patients who are in an unconscious state, under low
cranial nerve palsies, or incapable of mouth feeding due to some disease.The most
common conditions wanting RT Feed as a necessity include:
– Prematurity births,
– Failure to thrive or even extreme malnutrition cases,
– Several neuromuscular and neurologic disorders,
– Severe inability to swallow food, etc.
4)
although his hdl efects might be low HDL-33mg/dl , it does have significant for
his attack.the exact underlying mechanism of how low level
HDL-C might effect this condition is unknown.. However, it is well established
that HDL–C may protect against atherosclerosis by promoting cholesterol efflux
from macrophages in the artery wall. In addition, HDL-C may also reduce oxidation,
vascular inflammation and thrombosis, improve endothelial function, promote
endothelial repair, enhance insulin sensitivity and promote insulin secretion
by pancreatic beta islet cells [21]. One study postulated that
intracranial arteries have greater antioxidant enzyme activity compared to the
extracranial arteries
G) Link to patient details:
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
__*Questions*_
1)What is myelopathy hand ?
2)What is finger escape ?
3)What is Hoffman’s reflex?
AMISHA JAISWAL CASE
1) MYELOPATHY HAND;
A characteristic dysfunction of the
hand has been observed in various cervical spinal disorders when there is
involvement of the spinal cord. 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.
·
·
- cervical
myelopathy is a common degenerative condition caused by compression on
the spinal cord that is characterized by clumsiness in hands and gait
imbalance.
- treatment is typically operative as the condition is
progressive.
- Pathophysiology
- etiology
- degenerative cervical spondylosis
(CSM)
- most common cause of cervical myelopathy
- compression usually caused by anterior degenerative
changes (osteophytes, discosteophyte complex)
- degenerative spondylolisthesis and hypertrophy of
ligamentum flavum may contribute
- congenital stenosis
- symptoms usually begin when congenital narrowing combined
with spondylotic degenerative changes in older patients
- OPLL
- tumor
- epidural abscess
- trauma
- cervical kyphosis
- neurologic
injury
- mechanism of injury can be
- direct cord compression
- ischemic injury secondary to compression of anterior
spinal artery
- Associated conditions
- lumbar spinal stenosis
- tandem stenosis occurs in lumbar and cervical spine in
~20% of patients.
- CLASSIFICATION;stop,
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Usually
a significant improvement at 1-year po even in cases of severe myelopathy.
- 2)FINGER
ESCAPE SIGN;
·
- when patient holds
fingers extended and adducted, the small finger spontaneously abducts due
to weakness of intrinsic muscle.
- 3)HOFFMAN'S
REFLEX;
- Snapping patients
distal phalanx of middle finger leads to spontaneous flexion of other
fingers.
- Most common physical exam
finding.
- 6) Infectious Disease (HI virus,
Mycobacteria, Gastroenterology, Pulmonology) 10 Marks
A) Link
to patient details:
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
Questions:
1.Which
clinical history and physical findings are characteristic of tracheo esophageal
fistula?
2) What are the chances of this patient developing
immune reconstitution inflammatory syndrome? Can we prevent it?
1)CLINICAL HISTORY AND
PHYSICAL FINDINGS OF TRACHEOESOPHAGEAL FISTULA ARE;
CLINICAL HISTORY;
Cough and difficulty in
swallowing since 2 months initially with solids slowly progressed to liquids.
Wheeze in b/l mammary
areas
Laryngeal crepitus
-positive.
Barium study shows-
barium present in the bronchial tree through fistula.
Also crct has shown
that- there is fistulous communicationn between left main bronchus and mid
thoracic esophagus few cm below the carina.
Other causes might be;
She is rvd positive -in
these patients oeophageal candidiasis might be the cause for difficulty in
swallowing.
As she is tb positive -
any ulcers in the esophagous and enlarged lymphnodes that compress the
esophagous might be the cause.
2)IMMUNE RECONSTITUTION
INFLAMMATORY SYNDROME;
A
paradoxical clinical worsening of a known condition or the appearance of a new
condition after initiating antiretroviral therapy (ART) therapy in HIV-infected
patients resulting from restored immunity to specific infectious or
non-infectious antigens is defined as immune reconstitution inflammatory
syndrome (IRIS).
Because
clinical deterioration occurs during immune recovery, this phenomenon has been
described as immune restoration disease (IRD), immune reconstitution syndrome
(IRS), and paradoxical reactions.
Etiology of immune reconstitution inflammatory syndrome
OTHER MECHANISMS;
- The mechanism receiving the most
attention involves the theory that the syndrome is precipitated by the
degree of immune restoration following ART. An alternative immunological
mechanism may involve qualitative changes in lymphocyte function or
lymphocyte phenotypic expression. For instance, following ART an increase
in memory CD4+ cell types is observed possibly as a result of
redistribution from peripheral lymphoid tissue. This CD4+ phenotype is
primed to recognize previous antigenic stimuli, and thus may be
responsible for manifestations of IRIS seen soon after ART initiation.
After this redistribution, naïve T cells increase and are thought to be
responsible for the later quantitative increase in CD4+ cell counts.[4] Thus IRIS may be due to a combination of both
quantitative restoration of immunity as well as qualitative function and
phenotypic expression observed soon after the initiation of ART.
The
third purported pathogenic mechanism for IRIS involves host genetic
susceptibility to an exuberant immune response to the infectious or
noninfectious antigenic stimulus upon immune restoration. Although evidence is
limited, carriage of specific HLA alleles suggests associations with the
development of IRIS and specific pathogens.
Diagnostic Criteria for IRIS
French et
al., have laid down criteria so as to aid the diagnosis.[6] These are:
Major
criteria
- Atypical presentation of
“opportunistic infections (OI) or tumors” in patients responding to
antiretroviral therapy.
- Decrease in plasma HIV RNA level by
at least 1 log10copies/mL.
Minor
criteria
- Increased blood CD4+ T-cell count
after HAART.
- Increase in immune response specific
to the relevant pathogen, e.g. DTH response to mycobacterial antigens.
- Spontaneous resolution of disease
without specific antimicrobial therapy or tumor chemotherapy with
continuation of antiretroviral therapy.
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.
7) Infectious disease
and Hepatology:
Link to patient details:
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 ?
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 ?
4.What are the indications for ultrasound guided aspiration
of liver abscess ?
LIVER ABSCESS
1) YES, I THINK THERE IS CLOSE ASSOCIATION BETWEEN LOCALLY
MADE ALCOHOL AND LIVER ABSCESS.
Reasons
for this association between local alcohol beverages and ALA could be
multifactorial. Factors influencing the association could be related to the
pathogen, contents of beverages, status of the liver, and the immunity of the
host. They are more vulnerable perhaps due to the large infective dose of Entamoeba
histolytica and other bacterial pathogens ingested with the
unhygienically brewed beverage. Associated nutritional status of the population
and poor sanitation could also play a pivotal role. Hai et al. stated that
alcohol-induced hepatic dysfunction and possible suppression of amoebistatic
immune mechanisms by substances in the beverages could also be attributed in
the mechanism
ALA
almost always occurs in males with a history of drinking indigenously brewed
alcohol beverages in a poor socioeconomic background. As the primary
contributory factor is the male gender, we need to explore whether this gender
preponderance is purely due to alcohol-related factors or whether it is due to
other factors including the level of immunity of the host.
How
amoeba gets into the beverage is not well understood. Most likely this is due
to the unhygienic practices commonly seen at the drinking taverns or cottages
in many tropical countries. The important finding observed in most of the
studies is that majority of ALA patients are from a poor socioeconomic
background and are manual laborers [10, 6, 11]. Poor hygiene has been associated with increased
risk of amoebic liver abscesses and is directly proportionate to disease
progression and extent of liver injury [14]. Parasite cysts are transmitted through
contaminated food and water, making the incidence of disease high in areas of
poor sanitation. Good hygienic practices cannot be expected at these places as
the majority of subjects are male farmers from lower- and middle-class
backgrounds in one study [15] and 68% belonged to low socioeconomic group in
another study [11]. The prevalence of asymptomatic intestinal
amoebiasis is also common in these regions, although the prevalence rate varies
with the methods used for screening. It is high when microscopic examination
method is employed and low with the use of new molecular techniques [16]. It can be assumed that the regular visitors to
these drinking places could be the source of pathogen by unhygienic practices
including open air defecation, poor hand washing practices, unwashed utensils
at these taverns, and the consumption of unboiled drinking water. Indeed, some
studies have documented the prevalence of vectors of amoebiasis, including
flies and cockroaches at these places
2)ETIOPATHOGENESIS
OF LIVER ABSCESS IN CHRONIC ALCOHOLIC PATIENTS;
It is unknown why most
amoebic liver abscess (ALA) cases occur in alcohol drinkers. In experimental
studies, the presence of 'iron' potentiates the in-vitro growth of Entamoeba
histolytica (E. histolytica), and is also known to increase its in-vivo
invasiveness in animal infections. Chronic alcoholism increases the hepatic
iron deposition. We hypothesized that ALA occurs more commonly in livers with a
high iron load as in alcoholics. To test this hypothesis we compared the levels
of iron between ALA and non-ALA cases belonging to alcoholic and non-alcoholic
groups. Out of a total of 48 ALA cases, 34 (70%) were alcoholics and 14 (30%)
were non-alcoholics. After applying exclusion criteria, serum iron and liver
iron stores were quantified in 20 ALA cases (10 alcoholic and 10
non-alcoholics) and compared with 20 non-ALA cases (10 alcoholics and 10
non-alcoholics). All patients of ALA had serum iron values within the normal
range but higher than non-ALA cases. In the liver tissue, most patients with
ALA had higher (grade II or III) iron deposition, than non-ALA cases (mostly
grade I). Thus, patients with ALA, with or without alcohol indulgence, had
higher iron levels when compared to the non-ALA cases. It appears that the
higher incidence of ALA in alcoholic livers is possibly due to their higher
iron content.
3)LIVER ABSCESS IS MOST
COMMON IN THE RIGHT LOBE THAN IN THE LEFT LOBE;
LEFT LOBE RECIEVES BOOD FROM;
INFERIOR MESENTERIC AND SPLENIC VEINS
RIGHT LOBE RECIEVES BLOOD FROM
SUPERIOR MESENTERIC AND PORTAL VEINS.
STREAMING EFFECT INN
PORTAL CIRCULATION IS CAUSATIVE.
4)INDICATIONS FOR USG GUIDED ASPIRATION OF
LIVER ABSCESS;
Indications for
percutaneous drainage are broad: essentially any abnormal fluid collection in
the patient which can be accessible. Examples include:
·
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
Contraindications
The only common
contraindications are:
·
biopsy target is not accessible
·
patient has a bleeding diathesis
B) Link to patient details:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS:
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?
4) Is there a way to confirmthe definitive diagnosis in this
patient?
1) If
the cause is infectious, the majority of liver abscesses can be classified into
bacterial (including amebic) and parasitic sources (including hydatiform cyst)
Amoebic liver
abscess is an important cause of space-occupying lesions of
the liver; mainly in developing countries
Most amoebic infections are
caused by Entamoeba histolytica consumption of locally made alcohol (
toddy ) is the most likely cause of Liver abcess in this patient.
2)APPROACH TO LIVER ABSCESS;
3)
Considering the following
factors:
1) Age and
gender of patient: 21 years ( young ) and male.
2) Single
abcess.
3) Right
lobe involvement.
The abcess is most likely
AMOEBIC LIVER ABSCESS …
But most of the patients
with amoebic liver abcess have no bowel symptoms, examination of stool for ova
and parasite and antigen testing is insensitive and insensitive and not
recommended.
But most of the patients
with amoebic liver abcess have no bowel symptoms, examination of stool for ova
and parasite and antigen testing is insensitive and insensitive and not
recommended.
# And considering the
risk factors associated with aspiration for pus culture:
A)) Sometimes ; abcess is
not accessible for aspiration if it is in posterior aspect or so.
B)Sometimes ; it has thin
thinwall which may rupture if u aspirate.
C)Sometimes ; it is
unliquefied.
4) INVESTIGATIONS THAT
CAN BE DONE TO CONFIRM LIVER ABSCESS;
BLOOD CULTURES ARE POSITIVE
IN 50% OF CASES
CULTURE OF ABSCESS FLUID
CAN BE DONE.
ELISA CAN BE DONE
INDIRECT
HEAMAGGLUTINATION TEST-90%SENSITIVE
ULTASOUND-80-90%
SENSITIVE
CTSCAN-95-100% SENSITIVE
HEPATIC SCANS;
TECHNITIUM SCANS-80-90%
SENSITIVE
GALLIUM AND INDIUM SCANS
CAN ALSO BE DONE
8) Infectious disease
(Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks
A) Link to patient
details:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Questions :
1) What is the evolution of the symptomatology in this patient in terms of an
event timeline and where is the anatomical localization for the problem and
what is the primary etiology of the patient's problem?
A; Fever
since 10 days
Facial puffiness and
periorbital edema since 4 days
Weakness of right upper
limb and lower limb since 4 days
Altered sensorium since 2
days
2) What is the efficacy
of drugs used along with other non pharmacological treatment modalities
and how would you approach this patient as a treating physician?
A; as this patient is
diagnosed with acute oro rhino orbital mucormycosis with diabetes ketoacidosis-
the main stay of treatment would be liposomal ampotericin b according to
creatininnie clearance.
INDICATIONS;
- Empirical therapy for presumed
fungal infection in febrile, neutropenic patients.
- Treatment of Cryptococcal
Meningitis in HIV-infected patients
- Treatment of patients with Aspergillus species, Candida species
and/or Cryptococcus species infections (see above for the
treatment of Cryptococcal Meningitis) refractory to amphotericin B
deoxycholate, or in patients where renal impairment or unacceptable
toxicity precludes the use of amphotericin B deoxycholate.
- Treatment of visceral
leishmaniasis. In immunocompromised patients with visceral leishmaniasis
treated with , relapse rates were high following initial clearance of
parasites
MECHANISM OF ACTION;
SIDE EFFECTS;
Common side effects
of include:
- fever,
- shaking,
- chills,
- flushing (warmth, redness, or
tingly feeling),
- loss
of appetite,
- dizziness,
- nausea,
- vomiting,
- stomach pain,
- diarrhea,
- headache,
- shortness of breath,
- fast breathing 1 to 2 hours after
the infusion is started,
- sleep problems (insomnia), or
- skin rash.
SERIOUS SIDE EFFECTCS;
- swelling or pain at injection
site,
- muscle or joint
pain,
- unusual tiredness,
- weakness,
- muscle cramping,
- changes in the amount of urine,
- painful
urination,
- numbness or tingling of arms or
legs,
- vision changes,
- hearing changes (e.g., ringing
in the ears),
- dark
urine,
- severe stomach or abdominal pain,
- yellowing eyes or skin,
- swelling ankles or feet,
- fast/slow/irregular heartbeat,
- cold sweats,
- blue lips,
- easy bruising or bleeding,
- other signs of infection (e.g.,
fever, persistent sore
throat),
- mental/mood changes,
- seizures,
- black stools, or
- vomit that looks
like coffee grounds.
- APART FROM THIS PATIENT
IS DIAGNOSED WITH DIABETES KETOACIDOSIS WHICH HAS TO BE TREATED;
Managing diabetic
ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours
always is advisable. When treating patients with DKA, the following points must
be considered and closely monitored:
·
Correction of fluid loss with intravenous fluids
·
Correction of hyperglycemia with insulin
·
Correction of electrolyte disturbances, particularly potassium
loss
·
Correction of acid-base balance
·
Treatment of concurrent infection.
- REGULAR TREATMENT FOR
HYPERTENSION.
3) What are the
postulated reasons for a sudden apparent rise in the incidence of mucormycosis
in India at this point of time?
THE REASON FOR SUDDENRISE
IN THE INCIDENCE OF MUCORMYCOSIS MIGHT BE DUE TO THE INCREASED USE OF STEROIDS
IN COVID PATIENTS THAT LOWERS THR IMMUNITY
AND ALSO DUE TO INCREASED
INCIDENCE OF DIABETES ANDDIABETES KETOACIDOSIS.
Mucormycosis (sometimes called zygomycosis) is a
serious but rare fungal infection caused by a group of molds called
mucormycetes. These fungi live throughout the environment, particularly
in soil and in decaying organic matter, such as leaves, compost piles, or
rotten wood. 1
People get mucormycosis by coming in contact
with the fungal spores in the environment. For example, the lung or sinus forms
of the infection can occur after someone breathes in spores. These forms of
mucormycosis usually occur in people who have health problems or take medicines
that lower the body’s ability to fight germs and sickness. 3,6 Mucormycosis
can also develop on the skin after the fungus enters the skin through a cut,
scrape, burn, or other type of skin trauma.
Mucormycosis is rare, but it’s more common among
people who have health problems or take medicines that lower the body’s ability
to fight germs and sickness. Certain groups of people are more likely to get
mucormycosis, 1–3 including
people with:
- Diabetes, especially with diabetic
ketoacidosis
- Cancer
- Organ transplant
- Stem cell transplant
- Neutropenia pdf icon[PDF – 2 pages] (low
number of white blood cells)
- Long-term corticosteroid use
- Injection drug use
- Too much iron in the
body (iron overload or hemochromatosis)
- Skin injury due to surgery, burns,
or wounds
- Prematurity and low birthweight
(for neonatal gastrointestinal mucormycosis)
Types of
mucormycosis
- Rhinocerebral (sinus and brain)
mucormycosis is an infection in the sinuses that can spread to the
brain. This form of mucormycosis is most common in people with
uncontrolled diabetes and in people who have had a kidney
transplant. 7-8
- Pulmonary (lung)
mucormycosis is the most common type of mucormycosis in people with
cancer and in people who have had an organ transplant or a stem cell
transplant.
- Gastrointestinal
mucormycosis is more common among young children than adults,
especially premature and low birth weight infants less than 1 month of
age, who have had antibiotics, surgery, or medications that lower the
body’s ability to fight germs and sickness. 9-10
- Cutaneous (skin) mucormycosis: occurs after
the fungi enter the body through a break in the skin (for example, after
surgery, a burn, or other type of skin trauma). This is the most common
form of mucormycosis among people who do not have weakened immune systems.
- Disseminated mucormycosis occurs when the
infection spreads through the bloodstream to affect another part of the
body. The infection most commonly affects the brain, but also can affect
other organs such as the spleen, heart, and skin.
Types of
fungi that most commonly cause mucormycosis
Examples are: Rhizopus species, Mucor species, Rhizomucor species, Syncephalastrum species, Cunninghamella
bertholletiae, Apophysomyces species, and Lichtheimia (formerly Absidia)
species.
TREATMENT;
Mucormycosis is a serious infection and needs to
be treated with prescription antifungal medicine, usually amphotericin B,
posaconazole, or isavuconazole. These medicines are given through a vein
(amphotericin B, posaconazole, isavuconazole) or by mouth (posaconazole,
isavuconazole). Other medicines, including fluconazole, voriconazole, and
echinocandins, do not work against fungi that cause mucormycosis. Often,
mucormycosis requires surgery to cut away the infected tissue.
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