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Rough sheet for Rinky

 
 
 
 
Male patient with dysuria
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Take complete history
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Presence of urethral discharge
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes
 
 
 
 
 
 
No
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ask about the discharge
 
 
 
 
 
 
 
Presence Of Genital Lesion
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
YES
 
NO
Profuse,purulent discharge
Yellowish green colour
 
Thin,mucoid/mucopurulent discharge
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
SMEAR
 
SMEAR
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
FINDING
 
FINDING
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
GONORRHOEA
 
 
CHLAMYDIA
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 



















About 10 -15 percent of all cases of prion disease are caused by mutations in the PRNP gene.These form prion diseases are classified as familial prion diseases as they can run in families.It has overlapping signs and symptoms with familial Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), and fatal familial insomnia (FFI).

The PRNP gene provides instructions for making a protein called prion protein (PrP).The precise function of this protein is unknown, researchers have proposed roles in several important processes. These include the transport of copper into cells, protection of brain cells (neurons) from injury (neuroprotection), and communication between neurons.

In familial forms of prion disease, PRNP gene mutations result in the production of an abnormally shaped protein, known as PrPSc, from one copy of the gene. PrPSc can attach (bind) to the normal protein (PrPC) and promote its transformation into PrPSc,this process is not fully understood. The abnormal protein builds up in the brain, forming clumps which damage or destroy neurons. The loss of these cells creates microscopic sponge-like holes (vacuoles) in the brain, which leads to the signs and symptoms of prion disease.

Rest of the 85-90 percent of cases of prion disease are classified as either sporadic or acquired. People with sporadic prion disease have no family history of the disease and no identified mutation in the PRNP gene. Sporadic disease occurs when PrPC spontaneously, and for unknown reasons, is transformed into PrPSc. Sporadic forms of prion disease include sporadic Creutzfeldt-Jakob disease (sCJD), sporadic fatal insomnia (sFI), and variably protease-sensitive prionopathy (VPSPr).

Acquired prion disease results from exposure to PrPSc from an outside source. For example, variant Creutzfeldt-Jakob disease (vCJD) is a type of acquired prion disease in humans that results from eating beef products containing PrPSc from cattle with prion disease. This form of the disease in cows is known as bovine spongiform encephalopathy (BSE) or, more commonly, "mad cow disease." Another example of an acquired human prion disease is kuru, which was identified in population in Papua New Guinea. The disorder was transmitted when individuals ate affected human tissue during cannibalistic funeral rituals.

Rarely, prion disease can be transmitted by accidental exposure to PrPSc-contaminated tissues during a medical procedure. This type of prion disease, which accounts for 1-2 percent of all cases, is classified as iatrogenic.













  • In 1732, natural Scrapie- a slow infection of sheep caused by an unusual infectious agent was first described.
  • In 1957, the first prion disease in humans, Kuru-which is a fatal exotic neurodegenerative disease affecting only people of a single language group in the remote mountainous interior of New Guinea was described.
  • In 1959, veterinary pathologist W.J. Hadlow first recognized several similarities between Scrapie and Kuru.Kuru was described two years earlier by D.C. Gajdusek and V. Zigas. In the same year that Hadlow first proposed that Kuru and Scrapie might have similar etiology, I. Klatzo noted that Kuru's histopathology resembled that of Creutzfeldt-Jakob disease (CJD), another progressive fatal neurodegenerative disease of unknown etiology that A.M. Jakob had first described in 1921
  • Based on the knowledge of Scrapie, Gajdusek, C.J. Gibbs, Jr. and M.P. Alpers soon initiated efforts to transmit Kuru by inoculating Kuru brain tissue into non-human primates, that-although requiring several years-ultimately proved successful. Its transmissibility was demonstrated in 1965 by seminal work of Gajdusek, Gibbs and colleagues, followed by transmission of CJD and then,Gerstmann-Sträussler-Scheinker syndrome(GSS). Gajdusek and colleagues went on to demonstrate that not only the more common sporadic form of CJD but also familial CJD and a generally similar familial brain disease (Gerstmann-Sträussler-Scheinker syndrome) were also transmissible, first to non-human primates and later to other animals.
  • In 1982, Stanley B. Prusiner formulated "prion hypothesis". The work of S.B. Prusiner led to the recognition that a misfolded form of a ubiquitous normal host protein was usually (if not always) detectable in tissues containing TSE agents, greatly facilitating the diagnosis and TSEs, and understanding their pathogenesis. Prusiner proposed that the TSE agent was likely to be composed partly (if not entirely) of the abnormal protein, for which he coined the term "prion" protein and "prion" for the agent. Expression of the prion protein by animals-while not essential for life-was later found to be obligatory to infect them with TSEs.



Selection of therapeutic options through guideline-recommended treatment of asthma exacerbations has not been affected by what we currently know about COVID-19.

Systemic corticosteroids should be used to treat an asthma exacerbation per national asthma guidelines and current standards of care, even if it is caused by COVID-19. Short-term use of systemic corticosteroids to treat asthma exacerbations should be continued. There is currently no evidence to suggest that short-term use of systemic corticosteroids to treat asthma exacerbations increases the risk of developing severe COVID-19, whereas there is an abundance of data to support use of systemic steroids for moderate or severe asthma exacerbations. Patients with asthma but without symptoms or a diagnosis of COVID-19 should continue any required nebulizer for treatments, as recommended by national professional organizations.If healthcare providers need to be present during nebulizer use among patients who have either symptoms or a diagnosis of COVID-19, they should use recommended precautions when performing aerosol-generating procedures (AGPs). If clinicians are concerned that an asthma exacerbation is related to an underlying infection with COVID-19, clinicians can access laboratory testing for COVID-19 through a network of state and local public health laboratories across the country.

If patients with asthma who have symptoms or a diagnosis of COVID-19 need to use nebulizer at home,it is recommended by national professional organizations that they should use the nebulizer in a location that minimizes and preferably avoids exposure to any other members of the household, and preferably a location where air is not recirculated into the home (like a porch, patio, or garage) .Limiting the number of people in the room or location where the nebulizer is used is also recommended. Nebulizers should be used and cleaned according to the manufacturer’s instructions. If nebulizer use in a healthcare setting is necessary for patients who have either symptoms or a diagnosis of COVID-19, they must use recommended precautions when performing aerosol-generating procedures (AGPs).


Wastewater workers should use standard practices including basic hygiene precautions and wear the recommended PPE( Personal Protective Equipment) like goggles,protective face mask or splash-proof face shield,liquid-repellent coveralls,waterproof gloves,rubber boots as prescribed for their current work tasks when handling untreated waste.Basic Hygiene precautions include:

  • Washing hands with soap and water immediately after handling human waste or sewage.
  • Avoid touching face, mouth, eyes, nose, or open sores and cuts while handling human waste or sewage.
  • After handling human waste or sewage, wash hands with soap and water before eating or drinking.
  • After handling human waste or sewage, wash hands with soap and water before and after using the toilet.
  • Removing soiled work clothes before eating food and eating in designated areas away from human waste and sewage-handling activities.
  • Not smoking or chewing tobacco or gum while handling human waste or sewage.
  • Keeping open sores, cuts, and wounds covered with clean, dry bandages.
  • Gently flushing eyes with safe water if human waste or sewage contacts eyes.
  • Using waterproof gloves to prevent cuts and contact with human waste or sewage.
  • Wearing rubber boots at the worksite and during transport of human waste or sewage.
  • Removing rubber boots and work clothes before leaving worksite.
  • Cleaning contaminated work clothing daily with 0.05% chlorine solution (1-part household bleach to 100-parts water).


There are no additional precautions for HCP. Some HCP may choose to implement extra measures when arriving home from providing healthcare, such as removing any clothing worn during delivery of healthcare, taking off shoes, washing clothing, and immediately showering. However, these are optional personal practices because there is insufficient evidence on whether they are effective.People at higher risk of severe illness from COVID-19 should take the general precautions recommended for them which includes: Washing hands often, taking everyday precautions to keep space between them and others (stay 6 feet away, which is about two arm lengths),staying away from people who are sick,cleaning and disinfecting frequently touched services.


There is no evidence to suggest that employees of wastewater plants need any additional protections in relation to COVID-19.

Complications in Central Nervous System

  1. Cerebrovascular Accident
  2. Hemorrhagic
  3. Ischaemic
  4. Acute Encephalitis
  5. Viral Meningitis
  6. Epileptic Seizures
  7. Encephalopathy
  8. Headache

Complications in Peripheral Nervous system

  1. Guillain-Barre syndrome
  2. Anosmia
  3. Acute Myelitis
  4. Miller Fischer Sydrome
  5. Polyneuritis Cranialis

Ego defenses

Immature Defenses

  • Acting Out
    Expressing unacceptable feelings and thoughts through actions
  • Denial
    Avoiding the awreness of painful reality
  • Displacemnet
    Transferring avoided ideas to neutral persons
  • Idealization
    Expressing extreme positive thoughts of self and others while ignoring negative thoughts
  • Identification
    Modeling behaviour after one person who is more powerful.
These ego defenses are unconsious or conscious

DEFENSES
DEFENSES
Defenses

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Mature Defenses

  • Sublimitaion
    Replacing an unacceptable wish with a course of action that is similar to the wish but does not conflict with one's value system.
  • Altruism
    alleviating negative feelings via unsolicited generosity.
  • Suppression
    Intentionally withholding an idea or feeling.

18,Thursday,04,2024




Increased behaviour Decreased behaviour
Add stimulus (+)ve reinformation (+)ve punishment
Remove stimulus (-)ve reinformation


(-)ve punishment



Tumor nomenclature

Carcinoma implies epithelial origin,whereas sarcoma denotes mesenchymal origin. Both terms imply malignancy. terms for non-neoplastic malformations include hamartoma(disorganized overgrowth of tissues in their native location, eg, Peutz- Jeghes polyps) and choriostoma9 normal tissue in foreign location, eg, gastric tissue located in distal ileum in Meckel Diverticulum).

  • Benign tumor may show well demarcation, well diffreentiation, low mitotic activity, no necrosis, no metastasis.
  • Malignant tumor shows poor demarcation, poor mitotic activity, erratic growth, local invasion, metastasis, reduced apoptosis. Upregulation of telomerase prevents chromosome shortening and cell death.
CELL TYPE Benign
Malignant
Epithelium Adenoma,papilloma Adenocarcinoma, papillary carcinoma
Messenchmye
Blood cells lekaemia,Lymphoma
Blood vessels Hemangioma Angiosarcoma
Smooth muscle Leiomyoma Leiomyosarcoma
Striated muscle Rhabdomyoma Rhabdomyosarcoma
Connective tissue Fibroma Fibrosarcoma
Bone Osteoma Osteosarcoma
Fat Lipoma Liposarcoma
Melanocyte Nevus/Mole Melanoma



here is how we use reference




TYPE DEFINITION EXAMPLES STRATEGY TO REDUCE BIAS


Selection Bias Error in assigning subjects to a study group resulting in an unreprestative sample.Most commomnly a sampling bias
Berkson Bias
study population selected from hospital is less healthy than general population
Healthy worker effect
study population is healthier than the general population
Non-response bias
participating subjects differ from nonrespondents in meaningful ways.
randomization
Recall Bias Awareness of disorder alters recall by subjects; common in retrospective studies patients with disease recall exposure after learning of similar cases Decrease time from exposure to followup


Measurement Bias Information is gathered in a systemically distorted manner. Association between HPV and cervical cancer not observed when using non-standarized classifications/ Use objective, standardized, and previously tested methods of data collection that are planned ahead of time
Procedure Bias subjects in different groups are not treated the same patients in treatment group spend more time in highly specialized hospital units Blinding and use of placebo
Observer- expectancy Bias Researche's belief in the efficacy of a treatment changes the outcome of that treatment If observer expects treatment group to show signs of recovery, then he is more likely to document positive outcomes. Blinding



Heart Failure

Clinical syndrome of cardiac pump dysfunction-->congestion and low perfusion. Symptoms inlude dyspnea,orthopnea,fatigue; signs include rale,jugular venous distention(JVD),pitting edema.


Systolic Dysfunction
reduced EF,increased EDV;decreased contracility often secondary to ischaemia/MI or dialted cardiomyopathy
Diastolic Dysfunction
preserved EF, normal EDV;compliance often secondary to myocardial hypertrophy.



Caused BY Skin Preload CO Afterload Treatment
Hypovolumic hemorrhage,dehydration,burns Cold,clammy reduced reduced increased IV fluids
Cardiogenic Acute MI,HF Cold,clammy increased reduced Increased Inotropes, diuresis
Distributive Sepsis, anaphylaxis warm,dry reduced increased reduced IV fluids,pressors
  • this is how we add bullets
    • this is how layers
  1. this is how numbers are added

reference