Bimonthly Clinical Case Assignment 1
Bimonthly Clinical Case Assignment 1
Section 1) Please go through the patient data in the links below and answer the following questions:
1) Pulmonology (10 Marks)
A) Link to patient details:
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?
ANS: Evolution of symptomatology and Event timeline-
- 20 Years ago - SOB Grade1 for a week , occurred every year for the same duration
- 18 Years ago- Polyuria and was diagnosed with DM
- 12 Years ago - SOB Grade 1 for a month
- 1 Month ago - Weakness was giving IV
- 30 Days ago - SOB ( latest episode) gradually progressive
- 20 Days ago - HRCT showed Bronchiectasis
- 15 Days ago - Pedal edema and facial puffiness
- 2 Days ago - SOB Grade 4 , drowsiness and decreased urine output.
Primary etiology is rice dust exposure as patient is a farmer working in paddy fields.
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: Augmentin - Amoxicillin + Clavulanic acid.
MECANISM OF ACTION:
CLAVULANIC ACID
3) What could be the causes for her current acute exacerbation?
ANS:
- The pt. was started on antitubercular drugs even though she was tested negative for AFB. ATT includes drugs like ISONIAZIDE , RIFAMPACIN , ETHAMBUTOL , PYRAZINAMIDE AND STREPTOMYCIN .
- ISONIAZIDE can cause side effect like hypersensitivity reaction. COPD is a also an allergic which might have exacerbated due to use of isoniazide.
4. Could the ATT have affected her symptoms? If so how?
ANS: YES, some drugs like isoniazide could could acute exacerbation of COPD thereby increasing the symptoms.
5.What could be the causes for her electrolyte imbalance?
ANS:
COPD patients
- Electrolyte imbalance is found among people with Copd, especially for people who are female, 60+ old, take medication Spiriva and have High blood pressure.( this pt. is also hypertensive).
COPD patients present n
- Patients with COPD tend to retain sodium. In addition, serum potassium should be monitored carefully, because diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels.
- Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia.
- Activation of the renin-angiotensin-aldosterone system and inappropriately elevated plasma arginine vasopressin in COPD may aggravate the electrolyte imbalance during acute exacerbation of COPD.
2) Neurology (10 Marks)
A) Link to patient details:
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:
- 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 GABA a 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 mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological 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 in vivo 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?
ANS:
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?
ANS:
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 reason for kidney injury in this patient?
ANS:
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 anemia?
ANS:
Heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that cannot mature into functional cells. Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia(which is normocytic normochromic)
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
ANS: The pt. is already diabetic nd therefor formation of foot ulcer is high(macrovascular complication).In a patient of chronic alcoholic the immune system is weak due to the affect on blood cells formation and iron absorption, therefore , due to this healing of an ulcer dampens.
B) Link to patient details:
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?
ANS: Evolution of symptomatology:
- 7days back- H/O giddness with one episode of vomiting
- 4days back- H/O consumption of alcohol , following giddness and postural instability
- 4days back-Associated
with bilateral hearing loss, aural fullness, presence of tinnitus
- 4 days back- associated with vomiting 2-3 episodes.
- presents with slurring of speech, and deviation of mouth.
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 mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS:
- 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.
- 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.
- 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.
- 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.
- 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
- 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.
- Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
3) Did the patients history of denovo HTN 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 type of stroke?
ANS:
Atrial fibrillation and alcohol Drinking excessive amounts of alcohol can trigger atrial fibrillation – a type of irregular heartbeat. Atrial fibrillation increases your risk of stroke by five times, because it can cause blood clots to form in the heart. If these clots move up into the brain, it can lead to stroke.
C) Link to patient details:
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?
ANS: Evolution of symptomatology :
- 10 years ago- had an episode of paralysis attack on all four limbs( due to hypokalemia)
- 8 month ago- B/L pedal edema
- 7months ago- had blood infection
- 2months back- neck pain--diagnosed with cervical spondylosis
- 6days ago- left upper limb pain associated with tingling and numbness
- 5days ago- chest pain , palpitations and SOB
Primary etiology of the pt. problem of palpitation , chest pain and SOB is HYPOKALEMIA and for radiating pain of left upper limb is CERIVAL SPONDYLOSIS.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
ANS: The pt. is suffering with HYPOKALEMIC PERIODIC PARALYSIS.
Hypokalemic periodic paralysis (hypoKPP), also known as familial hypokalemic periodic paralysis (FHPP),[1] is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood. In individuals with this mutation, attacks sometimes begin in adolescence and most commonly occur with individual triggers such as rest after strenuous exercise (attacks during exercise are rare), high carbohydrate meals, meals with high sodium content, sudden changes in temperature, and even excitement, noise, flashing lights, cold temperatures and stress. Weakness may be mild and limited to certain muscle groups, or more severe full-body paralysis. During an attack, reflexes may be decreased or absent. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANS:
D) Link to patient details:
QUESTIONS:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
ANS:
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?
ANS:
First the pt. did not have LOC which might mean the pt. has focal seizer which could most commonly can be simple partial A/K/A focal seizers without impairment of awareness that is without LOC . Then the pt. has developed generalized tonic clonic seizers which is usually associated with LOC.
E) Link to patient details:
Questions:
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
ANS:
- This pt. is a chronic alcoholic who drinks few bottles per day which might have lead to multiple falls causing minor head injuries which he has always neglected and has not got it treated.
- These minor injuries must have been in cerebellar regions which over time lead to edema and damage and caused change in gait ( ataxia type of gait).
- Traumatic brain injury is a common cause of cerebellar damage. This type of injury is usually caused by situations such as automobile accidents, work injuries, or intentional blunt force trauma to the head. Some of the most frequently reported symptoms of damage to the cerebellum include slurred speech, loss of balance, and a lack of coordination.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
ANS:
- Analyses demonstrated an association of rare and moderate alcohol consumption with decreased risk of both lobar and nonlobar ICH. Heavy alcohol consumption demonstrated a strong association with increased nonlobar ICH risk.
- Study demonstrated potential protective effects of rare and moderate alcohol consumption on ICH risk. Heavy alcohol consumption was associated with increased ICH risk. Race/ethnicity was a significant factor in alcohol-associated ICH risk; heavy alcohol consumption in black and Hispanic participants poses significant nonlobar ICH risk.
F) Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
ANS: The RTA may have caused an internal brain injury or injury to any vessel which lead to ischemia which was left undiagnosed nd in mean time due to hypoxia turned into infarct.
there is also another possibility , that is RTA leading to brain injury which was treated at that time but incompletely . over time edema must have occurred or rupture of vessel due to any pressure effect leading to stroke.
traumatic head injury ( RTA in this case) :
2.What are warning signs of CVA?
ANS:
- Paralysis or numbness or inability to move parts of the face, arm, or leg - particularly on one side of the body
- Confusion- including trouble with speaking
- Headache with vomiting
- Trouble seeing in one or both eyes
- Metallic taste in mouth
- Difficulty in swallowing
- Trouble in walking (impaired coordination)
- Dystonia
- Alexia
- Agnosia
3.What is the drug rationale in CVA?
ANS:
4. Does alcohol has any role in his attack?
ANS:
Alcohol increases the risk of hemorrhagic stroke.
A hemorrhagic stroke occurs either when an aneurysm bursts, or a weakened blood vessel leaks. The result is bleeding either inside the brain, causing an intracerebral hemorrhage, or, less commonly, bleeding between the brain and the tissue covering it, causing a so-called subarachnoid hemorrhage.
The adverse effect of alcohol consumption on blood pressure – a major risk factor for stroke – may increase the risk of hemorrhagic stroke .
5.Does his lipid profile has any role for his attack??
ANS:
The lipid profile of the pt. is almost normal except HDLP which is little less. This pt. is neither hypertensive nor diabetic , so lipid profile having any role in attack is unlikely here.
But in general, Low HDL, High Homocysteine Predicts Poor Stroke Recovery For Diabetics. Patients with diabetes and low levels of HDL cholesterol, and high levels of homocysteine who have had a mild to moderate ischemic stroke were twice as likely as their counterparts without these conditions to have poorer cognitive function and greater disability after a stroke.
G) Link to patient details:
__*Questions*_
1)What is myelopathy hand ?
ANS: The “myelopathy hand” in cervical spondylosis includes findings of localised wasting and weakness of the extrinsic and intrinsic muscles of the hand
2)What is finger escape ?
ANS:
The finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign". Upper motor neuron disorders of the cerebral cortex such as mild hemiplegic stroke or hemiplegic migraine where the same clinical finding has been called the "digiti quinti sign".
3)What is Hoffman’s reflex?
ANS:
Hoffmann's reflex (Hoffmann's sign, sometimes simply " Hoffmann's ", also finger flexor reflex) is a neurological examination finding elicited by a reflex test which can help verify the presence or absence of issues arising from the corticospinal tract. It is named after neurologist Johann Hoffmann.
H) Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
ANS:
It might be cortical venous thrombosis according to the the results of imaging.
2) What are the risk factors for cortical vein thrombosis?
ANS:
Infections:
1.Meningitis, otitis,mastoiditis
2.Prothrombotic states:
3.Pregnancy, puerperium,antithrombin deficiency proteinc and protein s deficiency,Hormone replacement therapy.
Mechanical:
1.Head trauma,lumbar puncture
2.Inflammatory:
3.SLE,sarcoidosis,Inflammatory bowel disease.
4.Malignancy.
5.Dehydration
6.Nephrotic syndrome
Drugs:
1.Oral contraceptives,steroids,Inhibitors of angiogenesis
2.Chemotherapy:Cyclosporine and l asparginase
Hematological:
1.Myeloproliferative Malignancies
2.Primary and secondary polycythemia
Intracranial :
1.Dural fistula,
2.venous anomalies
Vasculitis:
1.Behcets disease wegeners granulomatosis
3)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.
4) 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 (10 Marks)
A) Link to patient details:
1.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.
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.
2.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.
3.What are the risk factors for development of heart failure in the patient?
ANS: IN THIS PATIENT:
- NON MODIFICABLE:
gender
smoking
type 2 diabetes .
kidney disease.
- MODIFIABLE:
smoking
type 2 diabetes .
kidney disease.
IN GENERAL RISK FACTORS:
4.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.
B) Link to patient details:
Questions:
1.What are the possible causes for heart failure in this patient?
ANS:
- obesity
- alcohol
- diabetes
- hypertension
2.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.
3.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 2 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.
4. 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.
C) Link to patient details:
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: Evolution of symptomatology and event timeline -
Past-
10yrs ago - Operation for Hernia
Since 2-3 yrs - Facial puffiness
1 yr ago - SOB grade II
1 yr ago - was diagnosed with Hypertension.
When the patient came to OPD -
Since 2 days - SOB which progressed from Grade II to Grade IV.
Since 2 days - Decreased urine output.
Since 1 day - Anuria
After admission -
CT scan - Showed dilated pulmonary vessels and thrombi in the atria.
2D Echo - Showed LV dysfunction.
Anatomical location - Atria (SA node)
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:
- Digoxin - It is a cardiac glycoside
MOA - It increases intracellular sodium that will cause an influx of calcium in the heart and cause an increase in contractility. It is vagomimetic.
Indications - Heart failure and arrhythmias.
- Carvediol - It is a beta-blocker.
MOA - It blocks the beta receptors and lowers the heart rate, blood pressure and strain on the heart.
Indications - Hypertension, heart failure, LV dysfunction with MI.
- Heparin - It is an anti-coagulant
MOA - It produces its major anticoagulant effect by inactivating thrombin and activated factor X through an antithrombin dependent mechanism. By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin induced activation of platelets and of factors V and VIII.
Indications - Prophylaxis and treatment of venous thromboembolism and pulmonary embolism; Atrial fibrillation with embolization ; chronic consumptive coagulopathies.
- Acitrom - It is an Oral anti-coagulant
MOA - It inhibits the reduction of Vitamin K by Vitamin K reductase. This prevents carboxylation of Vitamin K dependent clotting factors, II, VII, IX, X and interferes with coagulation.
Indications - Thromboembolic diseases such as DVT, Coronary occlusion
- Cardivas - It is an adrenergic blocker
MOA - Reversibly binds to beta adrenergic receptors on cardiac myocytes. Inhibition of these receptors prevent a response to the sympathetic nervous system, leading to decreased Heart rate and contractility
Indications - Hypertension, Angina and heart failure.
- Dytor - It is a diuretic. Contains Torsemide + Spironolactone
MOA - Through its action in antogonizing effect of Aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
Indications - Edema, Hypertension.
- Taxim - It is a cephalosporin antibiotic.
MOA - It is bactericidal through inhibition of cell wall synthesis.
Indications - Treatment of infections of throat, airway and urinary tract ; Typhoid fever.
- Thiamine - It is Vitamin B1.
MOA - Rapid restoration of Thiamine levels
Indications - Wernicke's encephalopathy, infantile beriberi etc.
- Inj. HAI - It is a short acting insulin.
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
ANS:
4) What are the risk factors for atherosclerosis in this patient?
ANS:
HTN, physical inactivity and obesity in this pt.
5) Why was the patient asked to get those APTT, INR tests for review?
ANS:
Anticoagulants being given to patient , therefore CVA and for predicting future ischemic attacks we do the above tests.
D) Link to patient details:
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?
ANS: Evolution of symptomatology :
- 12yrs ago- diagnosied with DM.
- 1yr ago - has heartburn like symptoms which are relieved without medication
- 7months ago- diagnosed with TB nd took treatment
- 6months ago- diagnosed with HTN
- 1/2 hour back- SOB grade 4
primary etiology is partial bloakage in coronary artery.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
TAB. METXL 25MG
mechanism of action
3) What are the indications and contraindications for PCI?
ANS:
INDICATIONS:
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term. Absence of cardiac surgery backup. Hypercoagulable state. High-grade chronic kidney disease. Chronic total occlusion of SVG. An artery with a diameter of <1.5 mm.
4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
ANS:
when PCI is performed in pt. who does not need it ..it lead to complications.
- Harms of over treatment:
Economy, Planet, Security, World and Health. But an epidemic of overtreatment — too many scans, too many blood tests, too many procedures — is costing the nation’s health care system at least $210 billion a year, according to the Institute of Medicine, and taking a human toll in pain, emotional suffering, severe complications and even death.
E) Link to patient details:
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?
ANS: Evolution of symptomatolgy:
- 8yrs back- diagnosed with DM
- 3 days back- developed chest pain radiating to back and dragging type
- since morning - giddiness and profuse sweating.
primary etiology is uncontrolled DM nd inferior wall MI
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
TAB. ASPIRIN 325 mg PO/STAT
TAB ATORVAS 80mg PO/STAT
TAB CLOPIBB 300mg PO/STAT
INJ HAI 6U/IV STAT
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
ANS:
starting PTCA after 12 hours is acceptable but after 3 days is not correct and can lead to complications.
4) Gastroenterology (& Pulmonology) 10 Marks
A) Link to patient details:
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?
ANS:
- 5years ago- developed pain abdomen and vomiting
- 1 week ago- developed pain abdomen
- 4days ago- developed fever , constipation and burning micturition.
Primary etiology of the condition is chronic alcohol intake.
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?
ANS:
- drugs used are meropenem , metrogyl , amikacin , octreotide and thiamine.
- 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.
- 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.
- 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.
- INJ.TRAMADOL
B) Link to patient details:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
ANS:
A sudden onset, severe upper abdominal pain in a patient looking very unwell is a very highly suggestive of pancreatitis. Occasionally, the patient may also have slight shortness of breath or painful breathing if the inflammation encroaches onto the lower part of the lung.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
ANS:
- Pancreatitis is nothing but the inflammation of the pancreas. Acute pancreatitis is caused when such an inflammation of the pancreas comes all of a sudden and brings the acute amount of pain.
- Pancreas that is mainly responsible for the production of the hormone, insulin. However, when the organ gets inflammation due to various reasons, the cells in the pancreas that are responsible for the production of the hormone are damaged. Thus, diabetes is caused. Thus, as a result of pancreatitis, a patient will require administering insulin through various external sources. The most common form of diabetes that is mainly known to be caused as a result of the pancreatitis is known as secondary diabetes.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
ANS:
- The liver is one of the largest and most complex organs in the body. It is the chief organ responsible for metabolizing alcohol and is especially vulnerable to alcohol related injuries.
- As alcohol is broken down inside the liver, it releases a number of potentially dangerous byproducts that may damage the liver more than the alcohol itself
- Each of these toxins plays a role in the damage of the liver and the subsequent release of enzymes from the cells
- Heavy drinking for as little as just a few days can lead to fatty liver, the earliest stages of alcoholic liver disease
4) What is the line of treatment in this patient?
ANS;
For the master chart to the "pancreatitis thesis project" please get in touch with Dr Shashikala PGY1 and Dr Divya PGY2 and share their insights into the above project problem they are working on.
C) Link to patient details:
Possible Questions :-
1) what is the most probable diagnosis in this patient?
ANS:
Ruptured liver abscess and hemoperitoneum.
2) What was the cause of her death?
ANS:
There is no true inflammation. (a) Acute onset type. Here sudden rupture of an amoebic liver abscess into the pericardium may result in a very severe shock and death within hours. Such cases can present with sudden retrosternal pain and shock with a previous history of epigastric pain and fever of few days' duration.
3) Does her NSAID abuse have something to do with her condition? How?
ANS:
drug induced hepatitis.
Drug-induced hepatitis is a redness and swelling (inflammation) of the liver. It is a rare condition caused by harmful (toxic) amounts of certain medicines, vitamins, herbal remedies, or food supplements. In most cases, you may be taking a medicine for several months before it reaches a toxic level and affects your liver.
5) Nephrology (and Urology) 10 Marks
A) Link to patient details:
1. What could be the reason for his SOB ?
ANS:
- Being short of breath can be related to the kidneys in two ways. First, extra fluid in the body can build up in the lungs. And second, anemia (a shortage of oxygen-carrying red blood cells) can leave your body oxygen-starved and short of breath.
- can it be because of dehydration as the pt. used diuretics ?
- here I am assuming kidney failure lead to diastolic dysfunction which lead to pulmonary congestion leading to SOB.
2. Why does he have intermittent episodes of drowsiness ?
ANS:
A decrease in the renal clearance of waste nitrogenous products accompanies with their continuous generation leads to diverse uremic retention products such as urea, creatinine, guanidine and homocysteine. Many of these toxins affect functioning of cells and organs, resulting in endothelial vascular injury, neurotoxicity and cognitive dysfunction.
Taken from the following article -
3. Why did he complaint of fleshy mass like passage in his urine?
ANS:
The fleshy mass like passage in his urine might be due to excessive pus cells in the urine (according to the reports) and the frothy appearance may be due to the presence of proteins. The urine is pale yellow in colour.
4. What are the complications of TURP that he may have had?
ANS:
- A complication of TURP that the patient may have had is 'TURP syndrome'.
- It is rare but is life threatening.
- Cause- It may occur as a consequence of absorption of fluids used to irrigate the bladder during the operation.
- Signs and symptoms are due to fluid overload and electrolyte disturbances and hyponatremia.
B) Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
ANS:
One possible Provisional diagnosis of this patient is ADHD (Attention deficit/Hyperactive disorder).
Symptoms may start before the age of 12 and include inattention and hyper active impulsive behavior.
Inattention -
They have trouble to stay focused in tasks or play.
They appear not to listen even when spoken directly.
They are easily distracted.
They avoid or dislike tasks that require mental effort.
Hyper active impulsive -
Have difficulty sitting in one place and are always on the run.
Fidget with their hands or legs.
Talk too much
Have difficulty waiting for their turn.
Academic difficulties are frequent as are problems with relationships.
2. Why doesn't the child have the excessive urge of urination at night time ?
ANS:
It maybe Psychosomatic. The child has the urge to urinate in the morning due to stress or mental conflict. During sleep, the kid is free of stress and may not have the urge to urinate excessively.
3. How would you want to manage the patient to relieve him of his symptoms?
ANS:
The only management is reassurance to the kid and his relaxation by reducing stress. The problem will resolve overtime (most commonly by the time he reaches 10yrs).
There are a variety of psychotherapeutic approaches employed by psychologists and psychiatrists; the one used depends on the patient and the patient's symptoms. The approaches include psychotherapy, cognitive-behavior therapy, support groups, parent training, meditation, and social skills training.
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology) 10 Marks
A) Link to patient details:
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
ANS:
- Clinical history- weight loss, recurrent chest infections, trauma, malignancy or ingestion of caustic substances, pyrexia of unknown origin
- Physical findings- Uncontrolled coughing after swallowing, often worse with carbonated drinks (ONO sign).
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
ANS:
7) Infectious disease and Hepatology:
Link to patient details:
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 ?
ANS:
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.
Though Alcoholism is a predisposing factor, it has no role in the aetiology and the liver function tests also did not show much alteration.
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
ANS:
Amoebic liver abscess is more common than pyogenic liver abscess. Commonly occurs in young alcoholic males.
Alcohol is only the predisposing factor of liver abscess but not the true etiological agent. Chronic alcoholism leads to Fatty liver and liver cirrhosis (Alcohol liver disease) which eventually results in liver abscess if liver is infected with entamoeba histolytica or other pathogenic organisms.
3. Is liver abscess more common in right lobe ?
ANS:
When the infection spreads to the liver through the portal veins it arises more commonly in the right lobe, probably due to an unequal distribution of superior and inferior mesenteric vein contents within the portal venous distribution. A plain abdominal radiograph is not sensitive for evaluating liver abscesses.
4.What are the indications for ultrasound guided aspiration of liver abscess ?
ANS:
1) If the abscess is large ( 5cm or more) because it has more chances to rupture.
2) If the abscess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.
3) If the abscess is not responding to the drugs for 7 or more days .
B) Link to patient details:
QUESTIONS:
1) Cause of liver abcess in this patient ?
ANS:
Cause of liver abcess may be due to contamination of food / fluid history of which is not mentioned.
malnutrition and poor personal hygiene are also the risk factors of liver abcess.
The cause for abscess in this pt. is infection with amoeba leading to amoebic liver abscess.
2) How do you approach this patient ?
ANS:
As mentioned earlier in practice we treat both pyogenic and amoebic liver abcess empirically.
* So we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.
* Next we administer patient with analgesic and antipyretic such as tab.dolo 650mg & tab.Ultracet , to relieve pain and fever.
##Abcess may get ruptured if untreated and cause peritonitis and shock.
3) Why do we treat here ; both amoebic and pyogenic liver abcess?
ANS:
we treat both pyogenic and amoebic liver abcess empirically beacuse we cant differentiate whether the abcess is because of bacterial infection or amoebic infecation.
So we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.
4) Is there a way to confirm the definitive diagnosis in this patient?
ANS:
Based on right hypochondriac and epigastric pain , fever
USG finding of hyperechoic mass in right lobe of liver along with other supportive investigations like leucocytosis (suggestive of infection/inflammation) and ALP ( Alkaline phosphatase ) rise in LFT is a suggestive diagnosis of LIVER ABCESS.
* Considering the following factors:
1) Age of the patient (21) - young & gender- male
2) Single abcess,
3) Right lobe involvement,
# The abcess is most likely to be AMOEBIC LIVER ABCESS.
We can also do USG guided aspiration to confirm the definitive diagnosis in this patient and also the stool culture.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks
A) Link to patient details:
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?
ANS:
- 3yrs ago - Hypertension was diagnosed
- 10days ago- Fever with chills and rigor
- 4days ago- facial puffiness and periorbital edema
- 4 days ago - weakness of right upper and lower limb
- 2days ago- altered sensorium.
Primary etiology: Mucormycosis is any fungal infection caused by fungi in the order Mucorales. Species in the Mucor, Rhizopus, Absidia, and Cunninghamella genera are most often implicated.
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?
ANS:
- itraconazole
- Deoxycholate ampB
- Inj. Liposomal amphotericin B
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
ANS:
- Mucormycosis was present even in the pre-Covid era, but is an opportunistic infection. The fungal infection is caused by a group of molds called mucormycetes. These molds live throughout the environment. Mucormycosis mainly affects people with damaged tissue or decreased immunity.
- The incidence of mucormycosis in India is around 14/100,000 population while that in Australia is 0.06/100,000 population. The reason behind this is India's hot humid climate where the spores of mucor survive for a longer time.
- When the sugars are not controlled, the increased level of sugar in blood provides acidic media which is a favourable environment for the growth of black fungus. Thus, the reason behind increased black fungus cases now can be attributed to uncontrolled diabetes and the use of drugs, which causes further decrease in immunity like steroids.As covid -19 positive pt. are being given steriods which is decreasing the immunity of body , thereby predisposing covid pt. to infection with black fungus.
9) Infectious Disease (Covid 19)
As these patients are currently taking up more than 50% of our time we decided to make a separate log link here:
for this question that contains details of many of our covid 19 patients documented over this month and we would like you to:
1) Sort out these detailed patient case report logs into a single web page as a master chart
2) In the master chart classify the patient case report logs into mild, moderate severe and
3) indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension etc).
Please check out the thesis log here for the example of a blogged master chart https://vamsikrishna1996.
10) Medical Education: (10 marks)
Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging of one's own experiences is a vital tool toward competency development in medical education and research. A sample answer to this last assignment around sharing your experience log of the month can be seen in the link below but while this is by a student onsite in hospital and not locked down at home we would be very interested to learn about your telemedical learning experiences from our hospital as well as community patients over the last month even while locked down at home: https://onedrive.live.
ANS:
It was a wonderful learning experience from all the cases we have seen online from our hospital. As of this covid-19 pandemic where we students are missing a lot of clinical practical learning session in person , due the efforts of our general medicine department , it is making a a lot of help to connect to subject as well as patients nd not waste our time. We are learning not only from and about on going pandemic related cases but also a lot about the other non covid-19 related cases .
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