General medicine case discussion
Online blended bimonthly assignment toward summative assessment for the month of May 2021
Name: preethi cheera
Roll no: 19
May 30 2021
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
This is the link of the questions asked regarding the cases:
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
PULMONOLOGY
CASE 1
A 55 Year Old Female with Shortness of Breath, pedal Edema and Facial Puffiness
Question no 1
what is the evolution of the symptomatology in this patient interms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient problem ?
Answer: 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 diabetis - 8yrs back
Anemia and took iron injections - 5yr ago
Generalised 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
Question no 2
what r the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patient?
2Answer:~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:non invasive method
#MOA :assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation9
3)Cause for current acute excerbation - it could be due any infection
4.could the ATT affected her symptoms if so how?
Yes ATT affected her symptoms
Isoniazid and rifampcin -nephrotoxic - raised RFT was seen
NEUROLOGY
CASE 2
A 40 Year Old Male with Complaints of Irrelevant Talking
A 40year old male presented with chief complaints of irrelevant talking and decreased food intake since 9days.
He was conscious but oriented to time, person and place only from time to time.
He also had short term memory loss since 9days, where he couldn't recognize family members from time to time
Previously, he had 2-3episodes of seizures, one being one year ago and the most recent being 4months ago. The most recent one, he had developed seizures following cessation of alcohol for 24hours.
1) what is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans: The patient is a chronic alcoholic, he drinks about 3-4quarters/day.he had developed seizures following the cessation of alcohol for 24hours it is due to the following reason:-alcohol affects the way in which nerve cells communicate. receptors are specialized proteins on the surface of nerve cells that receive chemical signals from one another. With long-term alcohol consumption, receptors affected by alcohol undergo adaptive changes in an attempt to maintain normal function.
Two important brain communication systems affected by alcohol involve the neurotransmitters:gamma-aminobutyric acid and glutamate.
The GABA system:
GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling. single doses of alcohol facilitate the inhibitory function of the GABA receptor, contributing to alcohol intoxicating effects. During withdrawal, brain GABA levels fall below normal and GABA activity declines. The combination of reduced brain GABA levels and GABAa receptor sensitivity may be contributed an adaptation to the presence of alcohol. In the absence of alcohol, the resulting decrease in inhibitory function may contribute to Symptoms of nervous system hyperactivity associated with both acute and protracted AW.
The glutamate system:
The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures. Alcohol inhibits the excitatory function of the NMDA receptor in laboratory studies at concentrations associated with mild to moderate alcohol intoxication in humans. As with the increased inhibitory function of the GABAA receptor, the decreased excitatory function of the NMDA receptor is consistent with alcohol’s general sedative effect. Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function. Persistent alterations in NMDA receptor function may potentiate the neurotoxic and seizure-inducing effects of increased glutamate release during withdrawal.
The symptom: irrelevant talking, decreased food intake, tremors, sleep disturbance is due to the following reason: chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver and other nutritional deficiencies.
THE PATHOPHYSIOLOGY:
Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.
The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease. The increase in levels of urea, creatinine, uric acid leads to uraemic encephalopathy. which causes asterixis.
the deficiency of thiamine and increase in levels of toxins in the body due to renal disease is the primary etiology of the patient's problem.
2)what are the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
Ans: I) Thiamine helps the body cells change carbohydrates into energy. It has been used
as a supplement to cope with thiamine deficiency
ii)Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.it enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
iii)pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.
iv)Lactulose is used in preventing and treating clinical portal-systemic encephalopathy .its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia.
v)Potchlor liquid is used to treat low levels of potassium in the body.
3)why have neurological symptoms appeared this time, that were absent during withdrawal earlier ? what could be a possible cause for this time?
Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.
4)what is the reason for giving thiamine in this patient?
chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine,Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine, and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death.
5)what is the probable cause for kidney injury in this patient?
The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease.
6)what is the probable cause for the normocytic anaemia?
alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron .alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption from intestine .
7)could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?
yes,As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic theimmune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.
CASE 3
A 52 year old male with Cerebellar Ataxia
NEUROLOGY
1) What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patients problem?
ANS. Timeline of the patient is as follows-
7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
H/O postural instability- falls while walking
Associated with bilateral hearing loss, aural fullness, presence of tinnitus
Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles
Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day
Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.
Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)
Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.
In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.
2) What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS.
A) Tab Vertin 8mg- This is betahistine, which is an anti- vertigo medication
MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
B) Tab Zofer 4mg- This is ondanseteron- It is an anti emetic
MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.
Indications- Used to control the episodes of vomiting and nausea in this patient.
C) Tab Ecosprin 75mg- This is aspirin. It is an NSAID
MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
D) Tab Atorvostatin 40mg- This is a statin
MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
F) Thiamine- It is vitamin B1
It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.
G) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
3) Did the patients history of denovo hypertension contribute to his current condition?
ANS. A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts.
Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?
ANS. Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.
Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain
Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subaracnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.
Many studies show that with mild and moderate drinking . the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
So In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition.
CASE 4
A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB
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?
A) *Evolution of symptoms :patient was normal 8 months back then developed b/l pedal edema which gradually progressed.
Aggerevated in sitting and standing position, relived on taking medication
*Palpitations :since 5days, sudden in onset which is more during night
Aggerevated by lifting heavy weights, speaking continuously
*Dyspnoea 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
Anatomical localisation :
Palpitations
Dyspnoea(NYHA-3)
Pedal edema
Chest pain
Radiating pain along her left upper limb
Etiological agent :
*By localization, electrolyte imbalance (hypokalemia) causing the her manifestations like palpitations, chest heaviness, generalised body weak ness
*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?
A) Reason: recurrent hypokalemic periodic paralysis
Current risk factor:due to use of diuretics
Other risk factors
A) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia
B) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
C) Inadequate intake: anorexia, dementia, stareation, total parental nutrition
D) psuedohypokalemia:delayed sample analysis, significant leukocytosis
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
A) 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.
CASE 5
55years old patient with seizures.
QUESTIONS:
1.Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury
Seizures after haemorrhagic strokes are thought to be attributable to irritation due to (hemosideri. Deposits)caused by products of blood metabolism
Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.
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?
Initially the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousness)
E) Link to patient details:
CASE 6
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