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a case presentation on diabetic foot/ case study on diabetic foot.martinshaji
This is a detailed study on diabetic foot a condition usually seen on patients with diabetics. this may become complicated according to the severity of the condition and diabetes , ideal management is needed with drugs sometimes surgical methods. this case study will give a detailed study about diabetic foot ............... the treatment, diagnosis , management, patient counselling, pharmacist intervention, pathophysiology etc
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how to examine sick baby , approach to child medical examination , diagnosis of sick child , evaluation of sick baby , medical examination of children , child medical history and examination , care of children
a case presentation on diabetic foot/ case study on diabetic foot.martinshaji
This is a detailed study on diabetic foot a condition usually seen on patients with diabetics. this may become complicated according to the severity of the condition and diabetes , ideal management is needed with drugs sometimes surgical methods. this case study will give a detailed study about diabetic foot ............... the treatment, diagnosis , management, patient counselling, pharmacist intervention, pathophysiology etc
Please leave a comment if you visited this
thank u
Long case examination done during MBBS and MD examination. Neurology case is mostly the long case. History, general examination , systemic examination, provisional diagnosis, investigation and final diagnosis are the sequential steps. Neurology examinations includes higher mental function, cranial nerve examination, motor and sensory system examination, cerebellar signs, gait, peripheral nerves, spine and skull and peripheral nerve examination.
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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2. RULES
• Each team will get 1 question in this round. A brief relevant
description of a clinical case will be provided. The description will
be followed by 2 questions pertaining to the case.
• Each team gets 2 minutes to work out on the case.
• There will be a brief Pounce window for the first 2 minutes. The
other teams can write their answers and it will be verified by the
QM, before the concerned team starts answering.
• The answers on pounce will be considered only if the team which
has the direct gets the diagnosis / questions wrong. Eg. If Team A
answers the diagnosis correctly but the questions wrong, only the
questions will be evaluated for pounce.
• Your diagnosis should be the most plausible one. The answers to
the subquestions should be to the point.
• In case of any discrepancy regarding the questions, the QM decision
is final.
3. POINTS
• Direct Question –
Diagnosis - +50/0
Questions - +20/0 each.
• On Pounce :
Diagnosis - +50/ -25
Questions - +20/ -10 each
PART POINTS ????? - Let’s see….
6. HISTORY
• A 36 year old female comes to the Emergency
department with sudden onset of severe abdominal
pain for the past 4 hours, with multiple episodes of
vomiting and bloody diarrhoea. The abdominal pain
has aggravated after the last meal she took. She is
also having Rheumatic Heart Disease, (untreated due
to financial constraints) Hypertension and
Dyslipidemia for the past 10 years. H/O Hospital
admission one year back due to complaints of
palpitations and dyspnea. The Patient is on Digoxin,
Warfarin, Amlodipine and Atorvastatin.
7. EXAMINATION
• O/E
Febrile - 100F SpO2 - 90%
Pulse - 120 bpm, feeble. BP - 90/46 mm Hg
CVS - S1 S2+, Mid diastolic Murmur + in mitral area.
RS - NVBS, Bilateral Crepitations +
• Abdomen - Soft, Tenderness elicited in umbilical,
hypochondrial, Right and Left Iliac fossa regions.
Guarding +
8. INVESTIGATIONS
ABG - Acidosis, Lactate levels, Urea, Creatinine high.
INR - 1.8 ( Inadequate control)
USG - No evidence of hemoperitoneum / blood
collection in the abdomen.
CT - Shows thickening of bowel wall, dilatation and
pneumatosis intestinalis.
9. QUESTIONS
• Most probable diagnosis?
1. Investigation of Choice for this condition?
2. Treatment Algorithm (basic)?
13. HISTORY
• A 55 year old male patient in RCC who is currently
undergoing combined chemo-radiotherapy for Non
Small Cell Lung Cancer, presents to EMS with acute
onset of chest pain, palpitations, confusion and
severe breathlessness. His comorbidities include
Hypertension and Type 2 Diabetes Mellitus. His
chemotherapy consists of Cisplatin with pemetrexed,
docetaxel and etoposide. Radiotherapy is of 60-66Gy.
No h/o past cardiovascular event / any abnormal
event during the course of therapy/ allergy to drugs.
14. EXAMINATION
Afebrile. Confused.
Pulse - 134 bpm, feeble, regular rhythm
BP - 78/40 mmHg
RR - 24 / min
CVS - S1 S2 present, but very low in intensity.
RS - Bilateral Crepitations seen. Use of accessory
muscles noted. Trachea in midline.
JVP - Raised.
Abdomen - Normal.
18. ANSWERS
• Diagnosis - CARDIAC TAMPONADE.
1. Pericardiocentesis – Paraxiphoid insertion of needle
at 15 Degrees towards the left scapula.
2. ECG features -
• Low voltage rhythm ( Amplitude <5 mm in limb
leads, <10 mm in chest leads)
• Beat to beat variation of QRS waves due to effusion –
ELECTRICAL ALTERNANS
20. HISTORY
• A 8 year old boy presents to the OPD with the chief
complaints of rash over the extremities for 6 days, abdominal
pain for 5 days and pain in the knee and ankle for 3 days. The
rash appeared initially on the thigh, but now is involving the
upper limb too. The patient describes the abdominal pain to
be moderate to severe in intensity with worsening of pain
after eating. One episode of stools mixed with blood
yesterday. The patient also reports a mild dull aching scrotal
pain for the past 2 days. No history of vomiting/fever/
headache. Past history reveals that the patient had an episode
of Upper Respiratory Tract Infection 3 weeks back. It subsided
after 3-4 days after treatment with Amoxicillin for 5 days.
21. EXAMINATION
• Conscious, Alert and oriented
Afebrile. Pulse - 92 bpm, BP - 134/90 mmHg.
CVS – S1S2+
RS - NVBS
CNS - Normal.
GIT - soft, no organomegaly. All orifices free.
Skin - Non blanching palpable purpura seen extending
along the entire length of the extensor surface of B/L
thigh, leg and arms.
22. INVESTIGATIONS
• USG Abdomen - Ruled out any intestinal perforation
/ intussusception.
Renal Function Test – Urine analysis showed
Proteinuria Grade + and Hemoglobinuria.
eGFR - 82 mL/min
Serum Creatinine - 1.6 mg/dL. Elevated urea levels.
23. QUESTIONS
• Diagnosis?
1. How will you confirm your diagnosis? What
will be its result?
2. What is the management of this condition?
25. ANSWERS
• Most Probable Diagnosis - HENOCH SCHONLEIN
PURPURA
1. Confirmation of HSP:
– Skin Biopsy – leukocytoclastic vasculitis with IgA
Deposition.
– Renal Biopsy – Mesangial thickening, proliferation
and deposition of IgA + C3
2. Treatment - Generally no treatment is required. However
if AKI + Oral Corticosteroids ( Prednisolone 1 mg/kg/d
over 2-3 weeks) + Analgesics can be given.
27. HISTORY
• A 50 year old man presents to the emergency with
acute onset of paralysis of right upper, lower limb
and deviation of mouth to right when he woke up
from sleep. He is accompanied by an attender, as he
is unable to speak. His attender gives history of past
episodes of stroke (total 3 in number) in the last 4
years which resulted in slurry speech, clumsiness of
hands, inability in dressing, urinary incontinence and
gait disturbances. He has also had left leg paresis
which has recovered moderately after physiotherapy.
28. HISTORY (contd)
• Past History reveals that the patient used to suffer
from episodes of severe unilateral migrane preceded
by aura since the age of 20. History of tonic-clonic
seizures since age of 25. Episodes - 4-5/year. H/o of
recent onset memory loss with inappropriate
behaviour and mood disorders also present. H/o
Hypertension for past 20 years. He is on Aspirin,
Phenytoin, Valproate, Amlodipine & Risperidone.
Family History - Father, Uncle and Nephew had
similar complaints. Father passed away due to stroke.
29. EXAMINATION
Patient conscious, alert, orientation not elicited.
BP - 190/125 mmHg. PR - 88 bpm. RR - 16 / min
CVS - S1S2 +
RS - NVBS.
CNS:
Higher Mental Functions - Aphasia +
Motor - Increased tone in right upper and lower limbs, Power
- 1/5 in both right UL and LL. Power - 4/5 on left side.
Exaggerated reflexes and Babinski's sign +ve on the right side.
Sensory - No perception of fine touch, crude touch,
temperature, vibration and pin-prick sensation in the right
upper and lower limbs.
Face - central weakness with sparing of the forehead. Mouth
deviated to right.
30. INVESTIGATIONS
• CT Brain - no signs of intracranial bleed. Multiple
small lacunar subcortical infarcts seen.
• MRI – not done
The patient was diagnosed as Acute Ischemic Stroke
31. QUESTIONS
• Diagnosis (Causative factor of the stroke) ?
1. What is the pathophysiology behind this
disorder?
2. Infarction of which area in the cortex produces
A. Urinary incontinence
B. Acalculia
•
35. HISTORY
• A 45 year old watchman presents to the OPD with
H/o cough and progressive dyspnea for the last 4
months. Cough is accompanied by expectoration
chunks of greasy solid sputum and increases on lying
down. Dyspnea is moderate and does not impair his
activities. H/o 2 episodes of pneumonia in the last 2
months resolved on taking Azithromycin for 5 days.
H/o Rheumatoid Arthritis for the past 2 years. H/o
Hypertension and DM-2. No H/o of anorexia/any
neckswelling/bone pain/weight loss/ exposure to
silica or asbestos. No H/o night sweats / evening rise
of temperature. No relevant family history.
36. EXAMINATION
Patient is conscious, alert and oriented.
Afebrile. BP - 150/90 mmHg. PR – 90 bpm
RR – 18 / min
Pallor + B/L Upper Limb Grade I Clubbing +
CVS – Normal
RS - Trachea midline, chest symmetric, normal
expansion. B/L coarse Crepitations + but no
increased vocal fremitus / resonance on percussion.
GIT - soft, non tender, mild splenomegaly.
37. INVESTIGATIONS
• Chest X-Ray - bilateral perihilar opacities. No air
bronchogram / cavitation / effusion /
consolidation / cardiomegaly
Histopathology - not done.
Hb - 10 mg/dL, no other CBC abnormalities.
ESR - elevated.
39. QUESTIONS
• Most probable Diagnosis?
1. What is the pathophysiology of this condition?
2. What is the typical sign on CT? Also mention
the treatment.
41. ANSWERS
• Diagnosis - PULMONARY ALVEOLAR PROTEINOSIS
(AUTOIMMUNE TYPE)
1. Presence of antibodies against GM-CSF leads to loss
of signaling and impaired differentiation of alveolar
macrophages – impaired ability to catabolize
surfactant, leading to surfactant accumulation
within the alveoli.
2. CT - Crazy Paving / Crazy Pavement sign.
Treatment – Steroids + GM-CSF.
44. HISTORY
• A 55 year old male presents to the OPD with the
symptoms of fever, weight loss and dragging
sensation in the left hypochondrium for 6 months.
Fever is low grade, no history of chills / rigors. H/o
recurrent upper respiratory tract infections. H/o
minor gum bleeds and nosebleeds for the past 3
weeks. Weight loss is > 10% and is accompanied by
anorexia. H/o night sweats for 4 months which
frequently drench the blankets. No H/o headache
/cough+expectoration /abdominal pain / diarrhoea/
vomiting / constipation / neck swelling. No family
history of similar complaints. H/o Diabetes Mellitus
for past 10 years.
45. EXAMINATION
• Concious, Alert and oriented.
Febrile - 99.6F
Pulse - 94 bpm, BP - 138 / 90 mmHg
Pallor + , No icterus / cyanosis / clubbing / edema /
lymphadenopathy
CVS - S1S2+
RS - B/L fine crepitations +
CNS - Normal
P/A - soft, non tender, massive splenomegaly noted (
touching the umbilicus) - 8 cm.
46. INVESTIGATIONS
CBC - Hb - 8 mg/dL, Neutropenia +, Platelets -
1,00,000/mm3, Microcytic Hypochromic Anemia.
Blood Smear - Presence of multiple cells with fine
projections, containing reniform nuclei and
threadlike extensions. MCHC Anemia.
Bone Marrow Aspirate - not adequate enough to be
processed.
Immunophenotyping - Positive for CD19, CD20,
CD11c, CD25.
CT Abdomen - Splenomegaly +, no infarcts, liver is
normal, no lymphadenopathy.
47. QUESTIONS
• Diagnosis?
1. What is the pathophysiology behind this disease and
the most classical infection associated with this
disease ?
2. What are the drugs used for treating the initial
presentation and recurrence of this disease?
49. ANSWERS
• Diagnosis – HAIRY CELL LEUKEMIA
1. Pathogenesis – Activating point mutations in BRAF
(due to substitution of valine with glutamate at
position 600 – V600E)
Most classical infection in Hairy Cell Leukemia -
Atypical Mycobacterial infections
2. Both initial presentation and relapse can be treated
with the same agents - Cladribine/Pentostatin +-
Rituximab