The skin is not only the largest organ of the body, but it also forms a living biological barrier with several functions.
Pyodermas are any pyogenic skin disease (has pus). Skin infections can be caused by bacteria (often Staphylococcal or Streptococcal) either invading normal skin, or affecting a compromised skin barrier
Some bacterial skin infections resolve without serious morbidity. However, skin infections can be severe and result in sepsis or death, particularly in vulnerable patient groups.
it is based on Harrisons and Davidson text book of internal medicine and Anathanarayanan textbook of microbiology. many clinical pictures have been embeded for better understanding. most common conditions seen in dermatology wards.
This seminar consisits of description of various bacterial diseases along with their oral manifestations,diagnosis and treatment.an addition of suitable case reports for better understanding and associated disorders
Cellulitis is a bacterial infection of the deep dermis and subcutaneous tissue. It is most commonly caused by S. pyogenes and S. aureus.5 Bacteria may gain access to the dermis via a break in the skin barrier in healthy adults, whereas the hematogenous route is more common in immunocompromised patients.
The affected skin is usually erythematous, swollen, painful, and warm to the touch. Severe cellulitis can be complicated by bullae, pustules, or necrotic tissue. Damage to lymphatic vessels can lead to recurrent episodes of cellulitis.6 In areas of the world endemic for lymphatic filariasis, it is important to rule out this disease in cases of recurrent bouts of lower-extremity cellulitis and lymphangitis.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The skin is not only the largest organ of the body, but it also forms a living biological barrier with several functions.
Pyodermas are any pyogenic skin disease (has pus). Skin infections can be caused by bacteria (often Staphylococcal or Streptococcal) either invading normal skin, or affecting a compromised skin barrier
Some bacterial skin infections resolve without serious morbidity. However, skin infections can be severe and result in sepsis or death, particularly in vulnerable patient groups.
it is based on Harrisons and Davidson text book of internal medicine and Anathanarayanan textbook of microbiology. many clinical pictures have been embeded for better understanding. most common conditions seen in dermatology wards.
This seminar consisits of description of various bacterial diseases along with their oral manifestations,diagnosis and treatment.an addition of suitable case reports for better understanding and associated disorders
Cellulitis is a bacterial infection of the deep dermis and subcutaneous tissue. It is most commonly caused by S. pyogenes and S. aureus.5 Bacteria may gain access to the dermis via a break in the skin barrier in healthy adults, whereas the hematogenous route is more common in immunocompromised patients.
The affected skin is usually erythematous, swollen, painful, and warm to the touch. Severe cellulitis can be complicated by bullae, pustules, or necrotic tissue. Damage to lymphatic vessels can lead to recurrent episodes of cellulitis.6 In areas of the world endemic for lymphatic filariasis, it is important to rule out this disease in cases of recurrent bouts of lower-extremity cellulitis and lymphangitis.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
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Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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2 Case Reports of Gastric Ultrasound
2. Bacterial Infection of Skin
Skin is largest organ of body. Maintains
homeostasis, protects underlying tissues
and organs, protects body from mechanical
injury, damaging substances, and ultraviolet
rays of sun.
3. • Two microorganisms are responsible for most
cutaneous infections in immunocompetent
patients:
• Beta-hemolytic streptococcus (groups A, B, C,
G, and F)
• Staphylococcus aureus, including community-
acquired methicillin-resistant S. aureus (CA-
MRSA).
4. S. aureus produces skin infection
I. Direct infection of skin and adjacent tissues
a. Impetigo
b. Ecthyma
c. Folliculitis
d. Furunculosis
e. Carbuncle
f. Sycosis barbae
II. Cutaneous disease due to effect of bacterial toxin
a. Staphylococcal scalded skin syndrome
b. Toxic shock syndrome
5. ß-hemolytic streptococcus
produces skin infection
I. Direct infection of skin or subcutaneous
a. Impetigo (non bullous)
b. Ecthyma
c. Erysipelas
d. Cellulitis
e. Necrotizing fascitis
II. Secondary infection
Eczema infection
6.
7.
8. Impetigo Contagiosa
• common superficial contageous
pyogenic skin infection.
•
two clinical forms
– Bullous impetigo.
– Non-bullous impetigo.
9. pathophysiology
• Bullous impetigo is caused by staphylococcus
aureus
• Non-bullous impetigo in majority caused
by S. aureus but can be caused by group A
beta hemolytic streptococci or both
10. Clinical features
• non-bullous impetigo,
• the initial lesion is a thin-walled vesicle on an
erythematous base which ruptures rapidly
• The exudate dries to form yellowish brown
crusts . Lesions enlarge and coalesce.
• The crusts eventually dry and separate to
leave erythema, which fades without scarring.
11.
12. • In severe cases
regional adenitis with fever and other
constitutional symptoms.
Sites
The face, around nose and mouth, and limbs
lesions may occur anywhere on the body,
especially in children with atopic eczema or
scabies.
tendency to spontaneous cure in 2,3 weeks
13. • In bullous impetigo, the bullae are less
rapidly ruptured and become much larger;
persist for 2 or 3 days
• some may become erosive
• Regional adenitis is rare
22. Management
• Impetigo is usually self-limiting and resolves
within days to weeks with the appropriate use
of topical cleansers and antibiotics.
• Spread to close contacts is common and
relapse is more frequently seen in individuals
with underlying skin diseases and in
staphylococcal carriers
23. • General measures:
Wash affected skin daily with disinfectants,
e.g. chlorhexidine, povidone iodine or sodium
hypochlorite.
• Handwashing for patient and close contacts.
• Localised disease: Topical antibiotics for
5–7 days, e.g. mupirocin, fusidic acid, or 2%
clindamycin cream
24. • Widespread or bullous disease or local
lymphadenopathy:
• Systemic antibiotics for 1 week.
• First-line antibiotics
flucloxacillin (dicloxacillin), cephalexin,
co-amoxiclav, cloxacillin and clindamycin.
• Second-line antibiotics
macrolides such as erythromycin and
clarithromycin
25. Ecthyma
• A pyogenic infection of the skin characterised
by ulceration with an adherent crust.
• Epidemiology
Extremes of age are most commonly affected.
• Pathophysiology
Causative organisms include GAS, Pseudomonas
aeruginosa and S. aureus.
26. • The infection is much deeper than in impetigo,
with loss of the epidermis and dermis,
ulceration and scarring.
• more common in immunocompromised
patients (HIV, diabetes, high humidity
environments and with poor hygiene.
• Pharyngeal carriers of S. pyogenes are more
susceptible to recurrent disease
28. Clinical features
• Small bullae or pustules on an erythematous
base are surmounted by a hard crust of dried
exudate
• predominantly on the buttocks, thighs and
legs.
• The crust can only be removed with difficulty
to reveal a purulent, irregular ulcer.
29. A large, circumscribed ulcer with a necrotic base and
surrounding erythema in the pretibial region
32. Management
• Improved hygiene and nutrition,
• treatment of scabies and any other underlying
disease
• Remove crust after soaking with a disinfectant
and softening with an oily cream.
• Topical antibiotics such as fusidic acid and
mupirocin
• Oral antibiotics (flucloxacillin or erythromycin) for
1–2 weeks
(multiple lesions or immunocompromised
patients)
35. Erysipelas
• bacterial infection of the dermis and upper
subcut tissue
• well-defined, raised edge
• reflecting more superficial (dermal)
involvement
36. Bacteriology
• Streptococci
• usually involving group A
• also G, C & B (esp setting of venous or lymphatic
compromise)
• Staphylococcus aureus
• occasionally alone or with a Streptococcus
• Haemophilus influenzae type b
• important cause of facial cellulitis in young Children
• rarely cellulitis in adults
37. Orbital cellulitis
• usually secondary to
sinusitis
• major sinus pathogens
• Streptococcus
pneumoniae
• Staphylococcus aureus
• Haemophilus influenzae
• penicillin-sensitive
anaerobes
56. Periorbital cellulitis
• follows trauma to the eyelids or local skin
sepsis .
• usually streptococcal
• occasionally staphylococcal.
• Complications
• cavernous sinus thrombosis,orbital, subperiosteal or
cerebral abscess formation, or meningitis
58. Investigations
• Swabs can be taken from vesicle fluid or
eroded or ulcerated surfaces
• blood cultures.
• In facial infections the pathogen should be
sought in nose, throat, conjunctiva and
sinuses.
59.
60. Treatment
• In all cases, initial treatment should
cover streptococci
• for facial infections in young children
initial treatment should cover, H.
influenzae (ceftriaxone, ceftazidime, cefotaxime, ampicillin-
sulbactam, fluoroquinolones, azithromycin)
61. Appropriate antibiotic(s)
• intramuscular or intravenous route
•more severe cases associated with
septicemia, arthritis or
suspected fasciitis
• oral treatment
•milder, uncomplicated infections
64. Recurrent cases
• Predisposing factors
– lymphatic damage
– Venous
insufficiency
– local skin damage
» T.Pedis
» Ulcer
• long-term Antibiotic
(some require lifelong)
• penicillin, 500 mg to 2 g daily
• Erythromycin
• Treatment of any local skin
damage
• eg T.Pedis
• Reduction of edema
65. Folliculitis
• Subacute or chronic inflammation of hair
follicles in which the inflammatory changes are
confined to the ostium or extend only slightly
below it
• heals without scar formation.
66. Folliculitis
• Its a superficial inflammatory disease of
hair follicle
• Mostly by staphylococci
• Caused by
Chemical irritants
Adhesive tapes, dressings
Occupational
Topical steroids
67.
68. • Dome shaped papules and pustules
• Mostly occur on beard area , face
• Can occur on thighs, buttocks and
extremities
75. Clinical features
• small, follicular, inflammatory nodule
• soon becoming pustular
• then necrotic
• healing after discharge of a necrotic core
• leave a violaceous macule
• Ultimately a permanent scar.
81. Carbuncle
• Deep infection of a group of
contiguous follicles with S. aureus
• Accompanied by intense
inflammatory changes in the
surrounding and underlying
connective tissues, including the
subcutaneous fat
82. Predisposing factors
• Middle or old age men
• Underlying disease
»Diabetes
»Malnutrition
»Cardiac failure
»Drug addiction
»Severe generalized dermatoses
- Exfoliative dermatitis
- Pemphigus
• Prolonged steroid therapy
87. Management
• Antibiotic
• Swab must be taken
• Incision drainage
• Diabetes and other possible
underlying conditions should
be sought
Editor's Notes
However, cellulitis may
extend superfi cially and erysipelas deeply, so that in many cases
the two processes coexist and it is impossible to make a meaningful
distinction. Current usage tends to regard erysipelas as a form
of cellulitis rather than a distinct entity, so that the defi nition of
cellulitis would include infl ammation of dermal as well as subcutaneous
tissue. The closely similar bacteriology of the two conditions
[1,2], and the demonstration of streptococcal antigens in both
dermis and subcutis in both conditions [1], support this view.
However, the two terms are still sometimes used in the traditional
sense, especially when their typical distinctive features are being
contrasted.
Haemophilus influenzae produces beta-lactamases, and it is also able to modify its penicillin binding proteins, so it has gained resistance to the penicillin family of antibiotics. In severe cases cefotaxime and ceftriaxone are the elected antibiotics, delivered directly into the bloodstream, and for the less severe cases an association of ampicillin and sulbactam, cephalosporins of the second and third generation, or fluoroquinolones. Macrolide antibiotics (e.g. clarithromycin) may be used in patients with a history of allergy to beta-lactam antibiotics.
[edit]Sequencing