MEDICAL ONLINE BLENDED BIMONTHLY ASSIGNMENT (MAY-2021)
MEDICINE ONLINE BLENDED ASSIGNMENT(MAY-2021)
Name:B.Shradha.
Rollno:10
8th semester
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, investigation and diagnosis and come up with the treatment plan.
This is the link of questions asked regarding the cases:
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1B
#NON-COVID CASES.
Below are my answers to the medicine assignment based on my comprehension of the cases.
PULMONOLOGY
CASE 1
1)A 55-year-old female with shortness of breath ,pedal Edema ,and facial puffiness.
a) EVOLUTION OF SYMPTOMATOLOGY:
#1st episode of SOB-20yrs back.
#2nd episode of SOB-12yr back.
#yrly episodes of SOB from past 12yrs.
#Diagnosed with diabetes-8yrs back.
#Aneamia &took fe injections-5yrs ago.
#Generalised weakness-1mnth.
#Diagnosed with HTN-20days back.
#pedal edema-15days back.
#Facial puffiness-15yrs back.
*anatomical localization of the problem is at the bronchioles.
etiology-its is due exposue of dust /allergens in paddy feilds
b)PHARMACOLOGICAL INTERVENTION:
*Head end elevation:
MECHANISM:In an intervention study involving early mobilization of intubated abdominal surgery patients, it was observed that high thoracic positions, such as sitting upright for 20 minutes, led to an improvement in transthoracic pressure, with consequent improvement in the Cst, rs. This gain enabled a reduction in the driving pressure required for the generation of a similar lung volume.
*BiPAP:
MECHANISM: During systole, CPAP induced increase in intrathoracic pressure reduces the venous return, decreasing the right and left ventricular preload, thereby improving mechanics in an overloaded ventricle, whereas in diastole, CPAP increases pericardial pressure, reduces transmural pressure, and thus decreases afterload.
*Augmentin(amoxicillin+calvulanic acid):
MECHANISM: Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes
*Azithromycin:
MECHANISM: Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit
*inj.lasix:
MECHANISM: Furosemide, like other loop diuretics, acts by inhibiting the luminal Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride, and potassium loss in urine.
*tab.Pantop:
MECHANISM: The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.
*inj. hydrocortisone:
MECHANISM:Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes. Hydrocortisone has a wide therapeutic index and a moderate duration of action.
*Neb. with ipravent ,budecortisone:
MECHANISM:
*Ipravent belongs to a group of medicines known as anticholinergic bronchodilators. Anticholinergic bronchodilators work by relaxing the bronchial tubes (air passages) that carry air in and out of your lungs. This makes breathing less difficult.
*Budesonide is a potent topical anti-inflammatory agent. [19] It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP
*tab.pulmoclear:
MECHANISM: Pulmoclear Tablet is a combination of two mucolytic medicines: Acebrophylline and Acetylcysteine. It thins and loosens mucus (phlegm) making it easier to cough out.
*chest physiotherapy:
MECHANISM:The aims of ACTs in patients with COPD are to assist sputum clearance in an attempt to reduce symptoms and paroxysmal coughing, slow the decline in lung function, reduce exacerbation frequency and hasten the recovery from exacerbations.
*inj.thiamine:
MECHANISM:thiamine may augment aerobic metabolism in the critically ill, even in the absence of absolute deficiency. We hypothesized that the administration of intravenous thiamine to critically ill patients would cause an increase in oxygen extraction and V.o2.
*BP,PR,SPO2,Temp:
MECHANISM: All 3 vital signs acquired from a pulse oximeter (pulse rate, oxygen saturation, and respiratory rate) are predictive of COPD exacerbation events, with oxygen saturation being the most predictive, followed by respiratory rate and pulse rate.
*I/O charting:
MECHANISM: Fluid overload or pulmonary/vascular congestion is a common clinical feature in patients with heart failure and is associated with adverse outcomes. Maintaining records of patients' fluid intake and output (I&O) has long been considered an important aspect of nursing care to assess hydration status.
c) The cause of acute Exaberation in this patient is probably due to generalised weakness due to the drugs or due to upper respiratory tract infection.
d)ATT could have effected the patient’s condition by causing generalised weakness.
e)*Hyponatraemia in COPD develops due to many reasons such as worsening of hypoxia, hypercapnia ,respiratory acidosis and right-sided heart failure with development of lower limb oedema ,it could also be due to renal insufficiency.
*respiratory acidosis with metabolic alkalosis( owing to renal compensation) in patients with COPD with hypercapnia is the usual cause of hypochloremia.
(2) NEUROLOGY
CASE 1
(A) A 40 year old male with complains of irrelevant talking.
a)Evolution of symptomatology:
#2009 (12 years ago): Started drinking alcohol
# 2019 (2 years ago): Diagnosed with Diabetes Mellitus, prescribed oral hypoglycemics
#2020 (1 year ago): Has an episode of seizures (most likely GTCS)
# January 2021 (4months ago): Has another seizure episode (most likely GTCS)- following cessation of alcohol for 24 hours. Starts drinking again after seizure subsides
# Monday, May 10, 2021: Last alcohol intake, around 1 bottle. Starts having general body pains at night.
# Tuesday, May 11, 2021: Decreased food intake. Starts talking and laughing to himself. Unable to lift himself off the bed, help required.
Conscious, but non coherent. Disoriented to time, person, place.Goes to an RMP the same day- is prescribed IV fluids and asked to visit a hospital
# Saturday, May 15, 2021: Is admitted to a tertiary care hospital for alcohol withdrawal symptoms, and is treated for the same.
#anatomical location and pathophysiology:
* Ethanol is a central nervous system depressant that produces euphoria and behavioral excitation at low blood concentrations due to increased glutamate binding to N-methyl-D-aspartate (NMDA) receptors; at higher concentrations, it leads to acute intoxication by potentiation of the gamma-aminobutyric acid (GABA) effects, particularly in receptors with delta subunits. The local distribution of these subunits explains why the cerebellum, cortical areas, thalamic relay circuitry, and brainstem are the main networks that mediate the intoxicating effects of alcohol.
*Prolonged alcohol use leads to the development of tolerance and physical dependence, which may result from compensatory functional changes by downregulation of GABA receptors and increased expression of NMDA receptors with production of more glutamate to maintain central nervous system (CNS) transmitter homeostasis
*Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate-mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures.The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits.
b) 1. IVF NS and RL
mechanism:Administer intravenous (IV) fluids for rehydration, as necessary. Most patients with severe alcohol withdrawal are significantly dehydrated, and their fluid requirements range from 4-10 L in the first 24 hours. Because hypoglycemia is common in these patients due to depleted glycogen stores, a 5% dextrose solution (in 0.90% or 0.45% saline) should be used to prevent hypoglycemia.
2. Inj. THIAMINE
mechanism:
*
It is well known that chronic alcoholics are at high risk for being deficient in vitamin B1 (thiamine), which is known to put the patient at an increased risk for Wernicke-Korsakoff Syndrome, cerebellar degeneration, and cardiovascular dysfunction.
What does thiamine contribute that allows the cells in the brain to respond to this metabolic demand?
Upon absorption into the body, thiamine is used to form thiamine pyrophosphate, which is an essential co-factor used by several cellular enzymes.
3. Inj. Lorazepam
mechanism:Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell.
4. T. Pregabalin
mechanism: Pregabalin is structurally related to the antiepileptic drug gabapentin and the site of action of both drugs is similar, the alpha2-delta (alpha2-delta) protein, an auxiliary subunit of voltage-gated calcium channels. 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.
5. Inj. HAI S.C.- premeal
mechanism:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
6. GRBS
mechanism:Regular blood glucose monitoring is an essential tool to help you take control of your diabetes. By identifying and recording changes in your blood sugar levels, you'll have more information about how food, exercise, stress, and other factors affect your diabetes.
7. glucose monitoring
mechansm:Regular blood glucose monitoring is an essential tool to help you take control of your diabetes. By identifying and recording changes in your blood sugar levels, you'll have more information about how food, exercise, stress, and other factors affect your diabetes.
8. Inj ampoule KCl
mechanism:Potassium ions participate in a number of essential physiological processes, including the maintenance of intracellular tonicity; the transmission of nerve impulses; the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of normal renal function.
9. Syp Potchlor
mechanism:It helps to maintain potassium balance in the body by restoring normal potassium levels in patients with a low level of potassium
c)Long-term abuse can damage the nervous system liver and other organs this damage maybe is reversible drinking too much alcohol can also alter the level of certain nutrients in the body including
* thiamine
* folate
* vitamin B6 and B 12
vitamins are needed for proper no function and can also cause alcohol related neurological diseases.
d) thiamine is used to form thiamine pyrophosphate, which is an essential co-factor used by several cellular enzymes.3 The pyrophosphate portion added to thiamine is important since this group is used to bind to magnesium and then further bind to amino acid side chains on the cellular enzyme.3 This allows the thiamin pyrophosphate to function as a co-factor to that enzyme so that it can facilitate the forward movement of its assigned biochemical reactions. One of the most important sets of biochemical reactions requiring the availability of thiamine includes the reactions involved in glycolysis and the tricarboxylic acid (TCA) cycle. There are three enzymes that facilitate several reactions involved in these processes that require the presence of thiamine pyrophosphate. These enzymes are a-ketoglutarate dehydrogenase, branched chain amino acid dehydrogenase, and pyruvate dehydrogenase. The forward movement of glycolysis and the TCA cycle are essential for the cell's ability to generate the ATP needed to maintain other cellular activity.
e)The sudden removal of alcohol can also cause kidney failure. Alcohol has to be broken down and cleared from the body as urine. This needs water, as the products of the breakdown have to be in solution.
Alcohol also inhibits the production of an anti-diuretic hormone, so large quantities of alcohol make you urinate a lot and become dehydrated. Electrolytes in the body, such as sodium, magnesium, calcium and potassium, are usually in solution (water) and excessive amounts of alcohol can cause an imbalance in these electrolytes as well as an acid-base imbalance. These imbalances can eventually lead to acute kidney failure.
f)the affected kidney leads to
1) a moderately reduced red cell life span,
2) blood loss, and
3) an inadequate increase in erythropoiesis relative to the fall in hemoglobin (Hb).
g)
excessive alcohol can cause nutritional deficiency and alcohol toxicity these in turn can cause poor nutrition leading to poor wound healing and problems with nerves (neuropathy) when sensory nerves in the foot stops working the foot can get injured and this leads to foot ulcers .
CASE 2
(B)A 52 year old male with Cerebellar Ataxia
a) Evolution of Symptomatology:
#7days back -developed giddiness.
#3days back again developed giddiness(sudden in onset, continous &gradually progressive).
#postural Instability-unavle
*the antomical location o the disease is CEREBREAL BLOOD VESSELS.
*the primary etiology is DENO HYPERTENTION in the patient.
b)PHARMACOLOGICAL INNTERVENTIONS
1)Tab Veratin
MECHANISM:
Betahistine is one of the few drugs known which is said to improve the microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action
(1) agonist of H1 receptors and
(2) antagonist of H3 receptors.
It has a weak effect on H1 receptors but strong effect on H3 receptors.
2)Inj Zofer
MECHANISM:
Zofer Tablet works by inhibiting the action of a chemical substance named serotonin, which is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea.
3)Tab Ecosprin
MECHANISM:
Ecosprin is an antiplatelet medicine. It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot.
4)Tab Atorvostatin
MECHANISM:
Atorvastatin is in a class of medications called HMG-CoA reductase inhibitors (statins). It works by slowing the production of cholesterol in the body to decrease the amount of cholesterol that may build up on the walls of the arteries and block blood flow to the heart, brain, and other parts of the body.
5)Tab Clopidogrel
MECHANISM:
The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
6)Inj Thiamine
MECHANISM:
Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
c)
Hypertension predisposes individuals to stroke by
(1) aggravating atherosclerosis in the aortic arch and cervicocerebral arteries; (2) causing arteriosclerosis and lipohyalinosis in the small-diameter penetrating cerebral end arteries; and
(3) promoting heart disease that may be complicated by stroke.
d)
*Liver damage due to too much alcohol can stop the liver from making substances that help your blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.
*alcohol consumption is associated with increased high density lipoprotein cholesterol levels, decrease platelet aggregation, increase fibrinolysis, and decrease plasma fibrinogen levels and this might help explain the lower risk of ischemic stroke
CASE 3
3)(C)
A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB
(a)what is the evolution of sympotmatology in this patient in terms of event timeline &where is the anatomical localisation for the problem &what is the etiology of patient problem?
Ans:- SYMPTOMATOLOGY:
patient was normal 8months back then developed bilateral peda edema.
.PAIN : since 6 days which is radiating along left upper limb.
.CHEST PAIN ASSOCIATED WITH CHEST HEAVINESS SINCE 5 days.
. PALPITATIONS : since 5days sudden onset more during night time and aggrevated by lifting heavy weights and speaking continuosly
. DYSPNEA: It is associated with palpitations since 5days
ANATOMICAL LOCALIZATION :-
chest pain, palpitations, DYSPNEA, pedal edema
By localization :
(Hypokalemia) electrolyte imbalance causing her manifestations like generalized body weakness radiating pain along her upper limb due to cervical spondylosis
(b)what are the reasons for reccurence of hypokalemia? Important risk factors for her hypokalemia
Ans:- Her recurrence of hypokalemia may be due to the use of diuretics.
Other risk factors like
Medications : diuretics, laxatives .
Osmotic diuresis, mineralocorticoid excess,
Malnutrition, alkalosis, Thyrotoxicosis.
(3) what are the changes seen in ECG in case of hypokalemia &associates symptoms?
Ans:-Hypokalemia results in slowe conduction, delayed ventricular repolarisation, shortened refractory period &Increased automaticity.
ECG CHANGES:-
Flattening and inversion of "T " Waves in mild hypokalemia, Decreased "T" Wave amplitude, "ST" Depression, prolonged "PR" Interval, visible "U" Waves .
Severe:- ventricular fibrillation , Rarely Av block.
SYMPTOMS OF HYPOKALEMIA:-
Muscle cramps, weakness, fatigue, anxiety, palpitaions, delirium, pain, psychosis.
c)Early changes of hyperkalemia include
tall,peaked T waves with a narrow base, best seen in precordial leads ;
shortened QT interval;
ST-segment depression. These changes are typically seen at a serum potassium level of 5.5-6.5 mEq/L
CASE 4
2(D)
55years old patient with seizures.
a). A stroke causes your brain to become injured. The injury to your brain results in the formation of scar tissue, which affects the electrical activity in your brain. Disrupting the electrical activity can cause you to have a seizure.
b)In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness Because due to progression of stroke there is will be scar formation s there will be worsening of symptoms leading to unconsciousness.
Abnormal increased activity in fronto-parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures. Abnormal decreased activity in these same networks may cause loss of consciousness in complex partial seizures.
CASE 5
2(E)A 48 year old male with seizures and altered sensorium
a)the reason for patient to develop ataxia in past one year is ALCOHOL
The toxic effects of alcohol are diverse. Alcohol-related cerebellar degeneration is one of the commonest causes of acquired cerebellar ataxia(ALCOHOL INDUCED TOXIC ATAXIA).
The pathophysiology remains unclear but proposed mechanisms include excitotoxicity, dietary factors, oxidative stress, compromised energy production and cell death
b)the reason for IC bleed is
CHRONIC ALCOHOL CONSUMPTION
↓
ALCOHOL INDUCED TOXIC ATAXIA
↓
REPEATED FALLS
↓
IC BLEEDING
* The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism and to the increased incidence and recurrence of gastrointestinal haemorrhage associated with excessive alcohol intake.
CASE 6
2(F)A 30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWER LIMB.
a)
The three main causes of a stroke following a car accident.:
The most common injury that car accident victims face is whiplash. This is caused by a collision with another car that severely and suddenly jerks your head and neck forward, resulting in the shredding of smooth muscle tissues. When the lining of arteries in your neck tears, it creates a large pressure of pooling blood that eventually gets trapped and forms a clot.
Hemorrhagic strokes, These types of strokes happen when blood from arteries seeps into the brain, usually a consequence of weakened blood vessels that rupture.
disruption of blood supply could trigger a stroke. If a car accident prevents a victim from being able to receive ample oxygen to the brain,
b)
WARNING SIGNS
FAST Sign
F for face If you notice a droop or uneven smile on a person’s face, this is a warning sign.
A for arms Arm numbness or weakness can be a warning sign. You can ask the person to raise their arms if you’re unsure. It’s a warning sign if the arm drops down or isn’t steady.
S for speech difficulty Ask the person to repeat something. Slurred speech can indicate that the person is having a stroke.
T for time If someone is experiencing stroke symptoms, it’s time to act fast.
Additional symptoms of stroke may include:
vision troubles, in one or both eyes
numbness in limbs, most likely on one side
overall fatigue
trouble walking
c)
PHARMACOLOGICAL INNERVENTIONS
1.Injection Mannitol
mechanism: Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
2.TAB Ecospirin
mechanism:Ecosprin provides the antiplatelet action by irreversibly inhibiting the formation of thromboxane A2, via acetylation of platelet cyclooxygenase. Thromboxane plays a role in the aggregation of platelets.
3.TAB ATORVAS
mechanism:In patients with recent stroke or TIA and without known coronary heart diseaseatorvastatin per day reduced the overall incidence of strokes and of cardiovascular events
Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
d)
in this case alcohol does not play a major role in cva as he drinks alcohol ocassionally.
e)
HDL (high-density lipoprotein), or “good” cholesterol, absorbs cholesterol and carries it back to the liver. The liver then flushes it from the body. High levels of HDL cholesterol can lower your risk for heart disease and stroke.
CASE 7
2(G)A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY
a)
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.
b)
Finger escape
Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".
c)
Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.
CASE 8
2(H).A 17 year old female with seizures
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
a)the cause of her condiion could be IRON DEFICENCY ANEMIA.
b)Risk factors for children and infants include:
Problems with the way their blood forms clots
Sickle cell anemia
Chronic hemolytic anemia
Beta-thalassemia major
Heart disease — either congenital (you're born with it) or acquired (you develop it)
Iron deficiency
Certain infections
Dehydration
Head injury
For newborns, a mother who had certain infections or a history of infertility
Risk factors for adults include:
Pregnancy and the first few weeks after delivery
Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation
Cancer
Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
Obesity
Low blood pressure in the brain (intracranial hypotension)
Inflammatory bowel disease like Crohn’s disease or ulcerative colitis
c)there was a sezuire free period due to administration of antiepileptic drugs as the effect of drugs weans off the sezures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the sezuires.
d)heparin as CLEXANE was given to relive clot in suspission of CVST
CARDIOLOGY
CASE 1
3(A).A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS
(A)
(1) what is the difference between heart failure with heart failure with preserved ejection fraction
and heart failure with reduced ejuction fraction?
Ans: HEART FAILURE WITH REDUCED EJECTION EJECTION FRACTION :- Also called
SYSTOLIC FAILURE
IT means heart (ventricles) is unable to contract properly which has to do it during ventricular
Systoli.sothe
Problem is failure in contractions of ventricles.
HEART FAILURE WITH PRESERVED EJECTION FREACTION :- Also called DIASTOLIC
SFAILURE IT means heart (ventricles) is unable to relax which has to do it during ventricular
diastoli. So the problem is failure in relaxation of ventricles
DIASTOLIC FAILURE :-
(a) Ability to receive blood during v. Diastoli decreased due to hypertrophied ventricle.
(b)CAUSES:-
systemic HTN, Aortic stenosis, pulmonary HTN, pulmonary stenosis, hypertrophic cardiomyopathy.
(c) In these patients
EDV decreases &EDP
Increases.
(d) Atria contrats against a stiffened Or hypertrophic ventricle produces heart sound S4.
SYSTOLIC FAILURE :-
(a) ventricular contractiona are weak whatever the amount of blood they recive during v. Diastoli they pump out less tha normal limit.
(b) CAUSES :-
. coronary artery disease, negative ionotropic drugs ( anti arrythmic drugs, beta blockers), copd/cor pulmonale.
(c) In these patients
EDV increases&EDP increases.
(d) Rapid ventricular filling in over filled ventricle produces heart sound S3.
3(B)
Questions:
(1) what are the possible causes for Heart failure in this patient?
Ans:- Diabetes 30years back and related complications like Diabetic neuropathy, nephropath, retinopathy are important risk factors for Heart failure.
HTN: Important risk factor
CHRONIC ALCOHOLIC:- LV dysfunction & Decresed LVEF
CKD,elevated creatinine
AST/ALT> 2 Also risk factors for heart failure.
(2) what is the reason for the anemia in this case?
Ans:As patient has developed diabetic nephropathy CKD -STAGE 4(chronic disease) patient may develop Anemia of because of decreases ERYTHROPOIETIN PRODUCTION.
Chronic infections, Inflammation leads to Increase in IL-6,IL- 8, TNF ALPHA.
THESE CYTOKINES ACTS ON
(a) BONE MARROW&(b) LIVER
(a) BONE MARROW :-
IN bone marrow they decrease ERYTHROPOIETIN PRODUTION, leads to decrease in RBC production, develops NORMOCYTIC NORMOCHROMIC ANEMIA.
(b) LIVER :-
IT increased HEPCIDIN,
Increases s. Ferritin , decreases transferrin, leads to MICROCYTIC HYPOCHROMIC ANEMIA.
HEPCIDIN Inhibits iron metabolism.
2.what is the reason for anaemia in this case?
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
4. What sequence of stages of diabetes has been noted in this patient?
CASE3
3(C).A-Fib and Biatrial Thrombus in a 52yr old Male
a)*the anatomical site is BLOOD VESSELS;
* ETIOLOGY:
The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.
b)PHARMACOLOGICAL INTERVENTIONS
1. TAB. Dytor
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
3. TAB. Cardivas
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C
MECHANISM:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.TAB. Digoxin
mechanism:
Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,
an enzyme that controls the movement of ions into the heart.
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
c)*cardiorenal syndrome type 4 is seen in this patient.
d)effect of hypertention
They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.
e)APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.
CASE 4
3(D)67 year old patient with acute coronary syndrome
https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1
a)*the anatomical site of etiology is BLOOD VESSLES
*Coronary artery disease is caused by plaque buildup in the wall of the arteries that supply blood to the heart (called coronary arteries). Plaque is made up of cholesterol deposits. Plaque buildup causes the inside of the arteries to narrow over time. This process is called atherosclerosis
b)
PHARMACOLOGICAL INTERVENTIONS
Met XL
MECHANISM:Tablet belongs to a group of medicines called long-acting beta-blocker. Met XL Tablet works by blocking the effects of some chemicals on your heart and blood vessels. It slows down your heart rate and helps it to beat with less force
Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis.
c)
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse. PCI is frequently reported to be overused and inappropriately recommended. Behnke et al defined overuse as ‘use of unnecessary care when alternatives may produce similar outcomes, resulting in a higher cost without increased value’.8Overuse causes a heavy financial burden on people living in countries, where fee-for-service and ill-regulated private healthcare provides much of the patient care. As a result, cost of healthcare increases and causes potential harm to the patients.
Factors responsible for percutaneous coronary intervention (PCI) overuse
Provider-related factors
Inappropriate PCI recommendation without coronary artery bypass grafting (CABG) facility availability.
PCI and diagnostic catheterisation performed during the same session (ad hoc PCI).
Lack of shared decision making.
Medico-legal concerns related to risks from failed medical intervention.
Poorly regulated, privatisation and fee-for-service in healthcare.
Fear of missing the ‘widow-maker’.
Patient related factors
Patient preference for minimally invasive PCI over CABG.
Lack of health literacy among patients.
Fear, anxiety, misperceptions and misbeliefs among patients about PCI benefits over optimal medical therapy and lifestyle modification.
CASE 5
3(E)CASE DISCUSSION ON ACUTE MYOCARDIAL INFARCTION
a)*the anatomical location ofetiology is BLOOD VESSELS.
*myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function
b)PHARMACOLOGICAL INNTERVENTION
1.TAB. ASPIRIN
mechanism:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.
2.TAB ATORVAS
mechanism:Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
3.TAB CLOPIBB
mechanism:The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
4.INJ HAI
mechanism:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.ANGIOPLASTY
mechanism:Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
c)
the second PCI was NOT necessary in this patient.
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
GASTROLOGY
CASE 1
4(A) A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA
a)*antomical location of etiology is pancreas(ductal obstruction,acinar cell injury,defective intracellular transport)
*The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes Attributed to alcohol
b)PHARMACOLOGICAL INTERVENTIONS
1) ING. MEROPENAM
mechanism:Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.
2) ING. METROGYL
mechanism:Metronidazole diffuses into the organism, inhibits protein synthesis by interacting with DNA and causing a loss of helical DNA structure and strand breakage. Therefore, it causes cell death in susceptible organisms.
3) ING. AMIKACIN
mechanism:he primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.
4) TPN ( Total Parenteral Nutrition )
mechanism: the early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infection; TPN is only required in a few patients.
5) IV NS / RL
mechanism:Patients with acute pancreatitis lose a large amount of fluids to third spacing into the retroperitoneum and intra-abdominal areas. Accordingly, they require prompt intravenous (IV) hydration within the first 24 hours. Especially in the early phase of the illness, aggressive fluid resuscitation is critically important.
6) ING. OCTREOTIDE
mechanism:
Like somatostatin, octreotide also decreases the release of growth stimulating hormones, decreases blood flow to the digestive organs, and inhibits the release of digestive hormones such as serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide.
Octreotide is useful in overdose management of sulfonylurea type hypoglycemic medications, when recurrent or refractory to parenteral dextrose. Mechanism of action is the suppression of insulin secretion.
7) ING. PANTOP
mechanism:The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.
8) ING. THIAMINE
mechanism:Vitamin B1 (thiamin) is indispensable for normal function/health of pancreatic cells due to its critical role in oxidative energy metabolism, ATP production, and in maintaining normal cellular redox state.
9) ING. TRAMADOL
mechanism:Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.
CASE 3
4(C).A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension
a)what is the probable diagnosis of this case?
#haemoperitonium might be the probable diagnosis
b)its possible for the blood to accumulate in the cavity extremly quickly.this could have caused her to go in shock from blood loss become unresponsive and may have resulted in death
c)NSAID abuse may have been the reason behind her hepatomegaly as they are known to
cause drug induced hepatitis which inturn leads to cirrhosis.
NEPHROLOGY
CASE 1
5(A)
1)POST TURP WITH NON OLIGURIC ANT DIABETIC NEPHROPATHY
A)
the reason for SOB was- metabolic acidosis .
CAUSE OF METABOLIC ACIDOSIS-
it is commonly found in patients with kidney disease(hydronephrosis) , and its causes are:
*impaired ammonia excretion
* reduced tubular bicarbonate reabsorption
* insufficient renal bicarbonate production in relation to the amount of acids synthesised by the body and ingested with food.
The respiratory center in the brainstem is stimulated, and hyperventilation develops in an effort to compensate for the acidosis.
b)*Acidosis has also been suggested to decrease muscle performance during fatigue by inhibiting Ca2+ release from the SR. Such inhibition will decrease the degree of activation of the contractile machinery and hence lead to decreased force production.
c)the cause of fleshy mass in urine might be due to papillary necrosis following hydronephrosis
d)complication of TURP that might have caused the disease could be
URETHRAL STENOS/BLADDER NECK STENOSIS
↓
BACKFLOW OF URINE INTO KIDNEY.
↓
HYDRONEPHROSIS
↓
PAPILLARY NECROSIS
Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
CASE 1
6(A)
A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH
a)
the clinical history and physical finding in this paient that suggest tracheoesophageal fistula is that ,Cough occurs on taking food and liquids
(which was initially non productive then associated with sputum which is white in color , moderate in quantity and non foul smelling)
b)Immune reconstitution inflammatory syndrome (IRIS) occurs in two forms:
"unmasking" IRIS refers to the flare-up of an underlying, previously undiagnosed infection soon after antiretroviral therapy (ART) is started;
"paradoxical" IRIS refers to the worsening of a previously treated infection after ART is started.
*Patients with mycobacterial disease at the time of initiation of ART are at higher risk of developing IRIS with an approximate risk of 15%. Patients originating from endemic areas for tuberculosis and cryptococcal disease are at higher risk of developing IRIS.
(b).
How can immune reconstitution inflammatory syndrome be prevented?
*The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
*Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.
*Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS.
INFECTIOUS DISEASE AND HEPATOLOGY.
CASE 1
7(A) LIVER ABCESS
a)
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.
b)
ETIOPATHOGENESIS
Etiology:
#Ascending cholangitis.
-Enteric gram negative Aerobic bacilli&Enterococci.
#Infections from pelvis &other Intraperitoneal sources
-mixed infestation with aerobic and non aerobic species.
-Bacteriodes Fragilis-Species ,most frequently Isolated.
#Hematogenous spread -by Staph.Aureus,S.Milleri.
c)50% of solitary liver abscesses occur in the right lobe of the liver (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.
the most common cause of liver abcess is pyogenic, which afftect lobe with more blood flow ie RIGHT LOBE
The right hepatic lobe receives blood from both the superior mesenteric and portal veins, whereas the left hepatic lobe receives inferior mesenteric and splenic drainage. It also contains a denser network of biliary canaliculi and, overall, accounts for more hepatic mass.
d)INDICATIONS FOR ULTRASOUND GUIDED ASPIRATION OF LIVER ABSCESS
Left lobe abscess not amenable to percutaneous drainage.
Life-threatening haemorrhage with or without intraperitoneal rupture of abscess
Amoebic abscess eroding into neighbouring structures
Septicaemia from secondary infection
Failure of response to conservative therapy.
CASE 2
CASE DISCUSSION ON LIVER ABCESS
7(B)
a)cause of liver abcess in this patient is ENTAMOEBA HISTOLYTICA
b)APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS:
# Use of Amoebicidal drugs like metronidazole is the 1st line treatment given.
#For pyogenic Abscess-Antiobiotics are prescribed.
#other treament options include-
(1) USG guided Aspiration of liver abcess.
(2) percutaneous drainage.
(3).surgical drainage.
c)we treat the paient for both amoebic and pyogenic abcess so that we dont rely only on anti-amebic therapy and insure comple treatment of the cause
d)he confirmatory test for amoebic abcess is Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).
*The diagnosis of amebic liver abscess was based on four or more of the following criteria:
(i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess,
(ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder),
(iii) enlarged and/or tender liver, usually without jaundice,
(iv) raised right dome of the diaphragm on chest radiograph, and
(v) improvement after treatment with antiamebic drugs (e.g., metronidazole).
CASE 3
8(A).50/Male came with altered sensorium
a)*the anatomical location of the problem is MAXILLARY SINUS
(primary disease is initiated in the upper or lower airways and is associated with the clinical development of sinusitis, rhinocerebral mucormycosis, )
*primary etiology of the patients's problem is IMMUNOSUPPRESSION CAUSED BY DIABETES MELLITUS.
b)PHARMACOLOGICAL INTERVENION
*inj.amphotericin B
MECHANISM:
Amphotericin B binds with ergosterol, a component of fungal cell membranes, forming pores that cause rapid leakage of monovalent ions (K+, Na+, H+ and Cl−) and subsequent fungal cell death. This is amphotericin B's primary effect as an antifungal agent.
*DEOXYCHOLATE AMPHOTERICIN B
mechanism:
Amphotericin B deoxycholate belongs to the polyene class of antifungals. It is also known by the name conventional amphotericin B and has been used for the treatment of invasive fungal infections
The addition of sodium dodecyl sulfate or sodium deoxycholate surfactant to modulate the aggregation state of Amphotericin B confirms that the monomer and dimer states have different fluorescence spectra.
c)Indiscriminate steroid usage and high blood sugar levels are potentially responsible for driving an uptick in a fungal infection among vulnerable COVID-19 patients.
:
4(B) PULMONOLOGY &GASTROENTEROLOGY.
(1) what is causing patient dyspnea? How is it related to pancreatitis
Ans:- There are multifactors causing dyspnea in pancreatitis due to pulmonary compliactions
(a) ACTIVATED TRYPSIN :-
Damage pulmonary vascultare and increases endothelial permeability.
Leads to formation clots in pulmonary circulation
(b)PLA2 ACTIVATION :-
PLA2 activated by trypsin
.Activation of PLA2 leads to removal of fatty acids from phospholipids .
. Phospholipids is a main component of lung surfactant(Dipalmitoylphoph-
-atidyl-choline) .
. These leads to decrese in lung surfactant production.
(c) PAF (Platelet activating factor) :-
. PAF regulates Interaction between PMNS (polymorphnuclear white cells) &endothelial cells facilitating migration of activated wbc in to the interstial spacesspaces in lungs.
(d)PRO- INFLAMMATORY CYTOKINES:-
Releases from pancreas such as TNF- ALPHA, IL-6, IL-8, IL-1, PMNS also contribute to release of cytokines.
(2) Name possible reasons why patient developed state of hyperglycemia
Ans:- IN ACUTE PANCREATITIS METABOLIC RESPONSE IS :-
a) Acute stress leads to Hyperglucagonemia that leads to hyperglycemia
b) Decreased release of insulin due to damage
Of pancreatic beta cells (due to Inflammation) leads to hyperglycemia.
(3) what is the reason for elevated LFT? Is there is a specific marker for Alcholic fatty liver disease?
Ans:- By the history patient is Alcholic. It suggests that elevated Lft are due to Alcohol consumption.
Elevated ALT& AST 1-4 times upper limits of normal in alcholic fatty liver disease.
(4) what is the line of treatment In this patient?
Ans :-
Investigations :
. 24 hour urinary protein
. Fasting and post prandial blood glucose.
. HbA1 c
. USG guided pleural tapping.
Treatment:-
.I.V FLUIDS 125ml/hr & ANALGESICS (TO reduce pain)
.Inj. Pantop
. I.V Antibiotics : only used if necrosis is present or confirmed infection.
Antibiotic of choice is MEROPENEM.
. Early initiation of enteral nutriotion should be done in pancreatitis it reduces mortality.
If patient cannot eat by mouth give enteral nutrition by naso gastric or naso jejunal route (naso jejunal route preffered).
. GRBS Charting 6th hourly
. BP charting 8th hourly.
(3) what is the reason for blebs &non healing ulcer in the patient
Ans:- (a) DIABETIC NEUROPATHY AND NEUROPATHY:-
Leading to hypothesis of an underlying associated loacal and sub basement membrane connective tissue attention and microangiopathy causing blisters.
MICROANGIOPATHY:-
Due to this narrowed blood vessels diabetic wound healing is impaired because less oxygen can reach the wound and tissues do not heal quickly
HIGH BLOOD GLUCOSE:-
when blood glucose is high impairs WBC function SO DECEASED IMMUNITY& body is unable to fight bacteria and close wound so wound healing is delayed.
POPLE WITH UNCONTROLLED DIABETES DEVELOP POOR CIRCULATION:-
AS circulation slows down blood moves slowly which makes it more difficult for blood to deliver nutrients to wound. As a result wound heals slowly.
(4) what sequence of stages daibetes has been noted in this patient
Ans :-stage 1:-INSULIN RESISTANCE.
Stage 2:-prediabetes
Stage 3:- Diabetes type -2
Stage 4:- Diabetic complications diabetic dermopathy, nephropathy, retinopathy, neuropathy.
INFECTIOUS DISEASES
(9)https://docs.google.com/spreadsheets/d/1DDu-XcyjVF6nbDSoxiqcIr5M0XwOfk1xBUfW2o8olto/edit?usp=drivesdk
(10)
Practice of medical education by preparing elogs and finding out Answers for the questions raised gives us more knowledge &makes the study of medicine very Interesting.It made me to learn New things daily on this platform.
#COVID CASES:
CASE-4
Covid 19mild:
1Q.Is elevated ESR due to covid related inflammation?
A.(1) Yes his evlevated ESR may be due to covid which indicates active inflammation status related to covid.
.His elevated ESR is 55mm 1st hour
2Q.What was the reason for this patients admission with mild covid?What are the challenges in home isolation and harms of hospitalization?
A.(2).if in a mild covid case there is sudden increase in cough and SOB -it indicates increase of infection in the lungs which may result in pnuemonia .
#In such case hospital admission is only the way to treat the pateint before the infection increases further.
*Challenges of home isolation:
1.pt sholud be clinicallu assigned mild /asymptomatic by treating medical officer.
2.A care giver should be available 24/7.
3.A.communicatiom link btw care giver and physician is pre requiste for entire duration of home isolation
4.Close contacts should be prescribed hydroxychloroquine as prophylaxis by the physician .
5.eldaerly pts (morethan 65)with comorbid conditions should be properly evaluted by the physician before allowing home isolation.
CASE -3
COVID 19 SEVERE
1Q.Why is noradrenaline given in this patient?
A.(1) As patient developed Acute kidney injury as complication due to covid and developed hypotension.
As noradrenaline is a vasopressor it is given to treat hypotension.
2Q.What is the Reason behind testing LDH levels in covid pts?
A.(2).If patient developed increased SOB which indicates progression of covid 19 disease to severe.
#LDH -is the predictor of respiratory failure in covid 19pts.
#IF LDH levels are elevated then it is associated with Greater than 16fold increase in odds of mortality.
#It is the useful tests for early identification of pts who req close monitoring.
3Q.why Patient switched from BIPAP to mechanical ventilation with intubation ?What are the advantages of it over the BIPAP?
A.(3).Bipap(bilevel positive airway pressure).
#machine used to pressurise air to higher level than the air in the room .
#It helps pt to inhale O2 and exhale CO2 more easily even while sleeping.
#mechanical ventilation with intubation is done in uncomsious pts or pts on aneasthetic.
#which allows the air to enter the lungs directly with out any respiratory effort by the patient
Adv of mechanical ventilation with intubation
# reduced work of breathing compared to spontaneous breathing.
#Gurantee delivery of set tidal volume .
#Allows limitation of peak inspiratory pressures .
#less interference with nrml cardiovascular. Functions.
#pt comfort and improved pt ventilator interaction .
CASE-9
Covid with denovo diabetes
2Q.Can it be a steroid induced diabetes which developed in the patient?
A.(2).usuage of steroids especially the large dose of dexamethasone which is used in severe cases of Covid -19 can lead to new onset diabetes.
#also result in an acute exacerbation of mild diabetes.
#by incresing the blood sugars by making the liver resistant to insulin.
#There is an entity called covid imduced diabetes.
CASE-12
Moderate to severe covid with prolonged hospital Stay
(1)What are the potential bioclinical markers in this patient that may have predicted the prolonged course of her illness?
Ans:The following biomarkers have been identified: hematological (lymphocyte count, neutrophil count, neutrophil–lymphocyte ratio (NLR)), inflammatory (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), procalcitonin (PCT)), immunological (interleukin (IL)-6 and biochemical (D-dimer, troponin, creatine kinase (CK), aspartate aminotransferase (AST)), especially those related to coagulation cascades in disseminated intravascular coagulation (DIC) and acute respiratory distress syndrome (ARDS). New laboratory biomarkers could be identified through the accurate analysis of multicentric case series; in particular, homocysteine and angiotensin II could play a significant role.
1Q.what are the known factors driving early recovery in covid?
Ans.
The sudden olfactory dysfunction is a common symptom in patients with COVID-19. Hyposmia patients recover more rapidly than anosmic ones while the middle age group carried the best prognosis in olfactory recovery. Females possess better potentiality in regaining smell after recovery and the association of comorbidities worsen the recovery rate of olfactory dysfunction in patients with COVID19.
13.Severe covid with 1st Diabetes.
1Q.what are the consequences of uncontrolled Hyperglycemia in covid patients?
Ans.clinical studies have found diabetes to be a major risk factor for disease severity and mortality [3, 4]. Patients with diabetes and/or uncontrolled hyperglycemia are more than twice as likely to be admitted to intensive care units (ICU) and mortality is up to three times higher compared to patients without diabetes and/or uncontrolled hyperglycemia [5].
It is well established that inpatient hyperglycemia, with or without known diabetes, contributes to a significant increase in morbidity, mortality, length of hospital stay, and healthcare costs, and that better glycemic control improves clinical outcomes [6,7,8]. This was also evident in prior coronavirus infection outbreaks like the severe acute respiratory syndrome (SARS) [9].
Several mechanisms have linked hyperglycemia to the worse prognosis of COVID-19. These mechanisms include those related to hyperglycemia and glycemic control as well as the impaired immune and inflammatory response caused by hyperglycemia [10]. Poor glycemic control has been associated with worse outcomes, including higher resource utilization, prolonged length of hospitalization, multi-organ injuries, and higher mortality [10,11,12,13]. Hyperglycemia in patients with and without diabetes can also have a negative impact on the efficacy of COVID-19 therapies, such as tocilizumab [14]. Frequent comorbidities associated with diabetes, such as obesity and hypertension, have also been associated with poor prognosis [15]. However, a recent study has shown that diabetes is associated with poor early outcomes among hospitalized patients with COVID-19, after adjustment for obesity [16]. In addition, accelerated respiratory deterioration has recently been identified as another mechanism whereby hyperglycemia can lead to worse outcomes of COVID-19 [17].
While some of these mechanisms remain to be elucidated, it seems clear that optimizing glycemic control can be crucial to improve COVID-19 outcomes. Well-controlled blood glucose (BG) levels, defined as BG between 70 and 180 mg/dL (3.9 and 10.0 mmol/L) have been associated with reduced medical interventions, major organ injuries, and all-cause mortality [11]. In fact, for every 10 mg/dL (0.6 mmol/L) drop in glucose levels between admission and 18 days, an 11% relative decrease in severe disease risk has been described in patients with hyperglycemia [10].
The limited data available suggest that glycemic control in patients with COVID-19 is inadequate. An observational study that evaluated glycemic control among hospitalized patients with COVID-19, diabetes, and acute hyperglycemia described 39.1% of BG values above 180 mg/dL (10.0 mmol/L) and 37.8% of the time of admission spent with a mean BG above 180 mg/dL (10.0 mmol/L) [12]. Another study showed 56.6% of capillary BG tests above the recommended target of 140–180 mg/dL (7.8–10.0 mmol/L) [18]. This may be due to high levels of stress, inflammation, a cytokine-mediated insulin-resistant state and lack of adequate protocols for glucose management [19]. It is also possible that the SARS coronavirus can penetrate into pancreatic islets and damage beta cells leading to insulin deficiency, thereby aggravating the course of diabetes and triggering acute hyperglycemia even in people without diabetes [20, 21]. This is supported by the observation of frequent cases of ketosis and severe diabetic ketoacidosis (DKA) at the time of hospital admission [22]. On the other hand, a rather large number or hypoglycemic episodes at hospital admission have also been reported, probably favored by COVID-19-induced anorexia without concomitant adaptation of glucose-lowering drugs [18, 20]. There are other factors associated with BG fluctuation that are especially relevant in patients with diabetes and COVID-19, such as the use of glucocorticoids, that can lead to large glycemic excursions which should be considered in setting the insulin pattern [23].
2)Does significance of elevated LDH indicates multi organ failure?
Ans:Lactate dehydrogenase (LDH) is an enzyme required during the process of turning sugar into energy for your cells. LDH is present in many kinds of organs and tissues throughout the body, including the liver, heart, pancreas, kidneys, skeletal muscles, lymph tissue, and blood cells.
When illness or injury damages your cells, LDH may be released into the bloodstream, causing the level of LDH in your blood to rise. High levels of LDH in the blood point to acute or chronic cell damage, but additional tests are necessary to discover its cause.
LDH test is most often used to:
Find out if you have tissue damage
Monitor disorders that cause tissue damage. These include anemia, liver disease, lung disease, and some types of infections.
Monitor chemotherapy for certain types cancer. The test may show if treatment is working.
(17)Covid -19with hypertension comorbidity.
1Q.How does hypertension effects the severity of covid Infection?
Ans:Pneumonia is the most common complication of the virus, it can also damage the cardiovascular system.
High blood pressure damages arteries and reduces the flow of blood to your heart. That means your heart has to work harder to pump enough blood. Over time, this extra work can weaken your heart to the point where it can't pump as much oxygen-rich blood to your body.
Coronavirus can also damage the heart directly, which can be especially risky if your heart is already weakened by the effects of high blood pressure. The virus may cause inflammation of the heart muscle called myocarditis, which makes it harder for the heart to pump.
If you also have plaque buildup in your arteries, the virus may make those plaques more likely to break apart and cause a heart attack. Past studies have shown that people with heart disease who get a respiratory illness like the flu or earlier types of coronavirus are at higher risk for a heart attack.
2Q.Causes of pleural effusion?
Ans:It is caused by fluid leaking into pleural space.
#This is from increased pressure in blood vessel /low blood protein count.
#pts with pneumonia are at increased risk for pleural effusion..
